CHRONIC KIDNEY DISEASE (CKD) HYPERTENSION:

Thickening of Afferent Arteriole

- Chronic renal failure
↓
- Pathological abnormality of the kidney
Decrease Renal Blood Floe
- Characterized by:
↓
o Hematuria
Decrease Filtration
o Proteinuria
↓
o Reduction of GFR / Creatinine clearance
Decrease GFR (kidney will produce renin)
≤ 60 ml/min
↓
- Irreversible
Activation of RAAS
↓
Causes of CKD:
Increase Heart Rate and Blood Pressure
1. Acutre renal failure
2. HTN - 2nd most cause
Notes:
3. Diabetes – most common cause
Chronic Activation of RAAS and thickening of AA would
- Diabetic nephropathy
cause damage to nephron and lead to glomerulo
4. Kidney disease
sclerosis (scar inside), there would be ischemia (loss of
- Cancer, obstruction
oxygenation).There is healing in portion but loss of
function.
ACUTE RENAL FAILURE
Pre renal Chronic: Glomerulosclerosis → Ischemia → death of
- Can cause renal artery stenosis (hardening) nephron
o No more contraction and dilation
- Heart failure HTN
- Hemmorhage - Loss of nephron
Which cause decrease the flow of blood going to the - Glomerular hyperfiltration lead to overworks
kidney ↓
↓ Sclerosis
Intra renal → CKD ↓
- Glomerulonephritis Too much death
- Acute tubular necrosis ↓
- Acute interstitial nephritis Decrease GFR
↑ ↓
Post renal Retention of waste
- BPH ↓
- Renal stone Toxic to the body
- Tumors
DIABETES
AKI/ARF CKD High blood sugar → ROS (free radicals)
↑ SC 0.3 mg/dl Hematuria ROS → activates growth factor
↑ SC 50% of baseline Proteinuria (Cytokines & oxidative stress)
Urine output < 0.5 GFR < 60 ml/min ↓
ml/kg/h for 6 hours Diabetic nephropathy
(changes in the nephron)
- hours to weeks - long standing
- reversible - irriversible
- can be CKD if left
untreated

5
 Loss of nephron = ↓calcitriol → ↓ ca reabsorption (GIT,
Kidney) → Hypokalemia → hyperparathyroidism →
breakdown of bones (bone resorption) →
OSTEODYSTROPY (nagiging weak ang bones)

Loss of nephron = ↓ GFR, other ions is not excretes

including PHOSPHATE
Thereby, ↑ phosphate it would activate parathyroid
hormone to have bone resorption
(HYPERPHOSPHATEMIA)

UREMIA
- Retention of nitrogenous waste in the blood
- AZOTEMIA (not severe) → Uremia
DIABETIC NEPHROPATHY - What would happen when there is uremia
1. Mesangial expansion o Neurologic problem
- Cannot filter well o Anorexia, vomiting
Mesangium o ↓of estrogen → amenorrhea
- Removes the trap residues of protein para o ↓ testosterone → impotence
kapag nagfifilter ang glomerulus maayos pa din o Skin changes (rashes)
- Keeping the filter free from debris - In the later sage
2. Podocytopathy o ↓renin → ↓ BP
o ↓EPO anemia → anemia
- Podocytes
o ↓ calcitriol → renal osteodystrophy
o Prevents protein from entering the
nephrons
3. Glomerular Basement thickening STAGES OF CKD
- Inflammation and scarring Stage GFR/ CrCl (ml/min)
- Can lead to nephron death 0 > 90
1 ≥ 90
CLINICAL MANIFESTATION 2 60-89
1. Na and H2O balance 3 30-59
- Dec GFR = Na & H2O retention → HTN → 4 15-29
Peripheral edema 5 (End-Stage
- Restrict fluid intake < 15
Renal Disease)
2. Potassium balance
- Dec GRF = increase K retention → (140 − 𝑎𝑔𝑒) × 𝑘𝑔
Hyperkalemia 𝐶𝑟𝐶𝑙 𝑚𝑎𝑙𝑒 =
73 (𝑠𝑒𝑟𝑢𝑚 𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒)
- Muscle weakness, arrhythmia (140 − 𝑎𝑔𝑒) × 𝑘𝑔
𝐶𝑟𝐶𝑙 𝑓𝑒𝑚𝑎𝑙𝑒 = × 0.85
- Loss of nephron = ↓renin production = 73 (𝑠𝑒𝑟𝑢𝑚 𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒)
↓aldosterone → DCT will not work → K RISK FACTORS
retention 1. age > 50 y/o
- DO NOT USE K SPARING DIURETICS & ACE 2. HTN
INHIBTOR 3. Male gender
3. Metabolic acidosis 4. African American / Hispanic race
- ↓ capacity to excrete H ions and generate 5. Family history
bicarbonate → acidosis 6. Smoking
7. Obesity
- Acidosis leads to bone decalcification
8. Long term analgesics (NSAIDS)
4. Kidney
9. Diabetes
- Release renin, erythropoietin, calcitriol 10. Auto immune disease

6
COMMON SIGNS & SYMPTOMS - STATINS: additional therapy: has
1. Fatigue cardioprotective effect in px with CKD and
2. Anemia → dec EPO in < 50 ml/min cardiovascular disease.
3. Edema – Na & H2O retention o GOAL: LDL <70mg dL
4. Nausea & pruritus – accumulation of waste product o Non-dihydropine CCBs
5. Infection  For patient experiencing cough,
6. Arthralgia – masakit ang joints angioedema, hemodynamic decline
of renal function and hypokalemia
OTHER DIAGNOSTIC FACTORS  Has more proteinuric-lowering effect
1. BPH than other antihypertensive agents
2. Foaming appearing urine (protein) o STATINS: additional theraoy for cardio
3. Cola color urine protection
4. Rashses - Adjunct therapy
o If the target BP is not achieved with the
use of non-dihydropyridine CCB
CLINICAL INDICATOR
o HCTZ: maximum of 50 mg/day
1. Microalbuminuria
o Atenolol: max. of 25-50 mg/day
2. Proteinuria > 300 mg//day
o Metoprolol: max. of 100 mg.day
3. Hematuria
o SECONDARY OPTIONS:
 Aliskiren – renin inh
STAGES OF RENAL DYSFUCTION  Hydralazine – vasodilator
Metabolic Action
Stage Description GFR  Minoxidil – vasodiator
consequence Plan
1 Normal or ↑ >90 At ↑ risk of CKD: 1. Screen  Clonidine – a2 agonist
GFR- people 1. HTN for CKD
with ↑ risk or 2. Diabetes risk Metabolic
Stage Description GFR Action Plan
with early 3. Obesity 2. Establish consequence
renal damage diagnosis 3 Moderate 30- • Decreased • Monitor
3. Treat renal failure 59 calcium GFR monthly
underlying (CRF) absorption • Avoid
diseases (GFR <50) nephrotoxic
4. Retard • Lipoprotein drugs
progression activity falls • Prescribe
2 Early renal 60- Concentration of 1. Control • Malnutrition antiprotenuric
insufficiency 90 parathyroid BP • Onset of drugs
hormone starts 2. Control anemia (↓EPO) •ACEI or
to rise DM ARBs
3. • Adjust drug
Protenuria dose
reduction
STAGE 3
Treatment:  Identidy co morbidities such as anemia and
For stage 1 and 2 WITHOUT UREMIA: secondary hyperparathyroidism
- ACE inhibitor / ARBS  Anemia maybe treated with erythropoietin
o If px has proteinuria > 500mg/day: reduce replacement if Hb falls to <1-g/dL
BP to <125/75 mmHg and proteinuria to < o Target Hb: 11-12g/dl
500 mg/day  Hyperparathyroidism, calcium phosphorus levels
o ACEI and ARBS are the first line treatment should be intact
for controlling BP to a goal and proteinuria o Dietary restriction and/or phosphate
is < 500mg/day, control BP to a goal of binding medications
<130/80mmHg
- Both drugs are associated with hyperkalemia in
patients with acute renal failure, this is
reversible once medication has been
discontinued.

7
 Metabolic STAGE 5 with UREMIA
Stage Description GFR Action Plan
consequence  First line: Dialysis
4 Severe renal 15- • Triglyceride • - Renal replacement therapy is initiated once
failure (Pre- 29 concentrations Preparation
End stage start to rise for renal patient has stage 5 and or signs of uremia
renal failure) • Hyper replacement o Weight loss
phosphatemia therapy o Lack of appetite
• Metabolic o Nausea
acidosis o Acidosis
• Tendency to o Hyperkalemia
produce
hyperkalemia - Peritoneal dialysis: peritoneal catheter is
inserted in the abdomen
STAGE 4 - Haemodialysis: prescribed 3 times a week for 4
 Educate px about renal replacement therapy hours each session
such as dialysis and kidney transplantation  Second line: Kidney transplantation
 Kidney transplantation is recommended once
GFR falls under <20mL/min Treatment for the underlying risk factors:
 Parathyroid hormone with active vitamin D3  Glycemic control
must be maintained at 70-110 nanograms/L  Goal of BP: <130/80 mmHg with ACEI/ARBs
 <125/75 for patients with proteinuria >
TREATMENT FOR STAGE 3 500mg/day
 ACEI/ ARBS  Tobacco cessation
 STATINS  Protein restriction in stages 4 & 5
 ADJUNCT
 NOTE: ALISKREN + ACEI/ARBS is FOLLOW UP RECOMMENDATION
contraindicated to patients with diabetes Monitoring
because of the risk of renal impairment, - Annual evaluation of serum creatinine
hypotension, hyperkalemia - Estimation of GFR
 Avoid also in patients with moderate to severe - For Established CKD
renal impairment. - Rate of progression should be serially assessed
 Patients with ANEMIA starting Stage 3
- ADJUNCT: recombinant erythropoietin - Screening anemia and bone mineral disorders at
therapy least every 6 months
 Erytropoeitin Alfa - Annual lipid profile
 Patients with SECONDARY
HYPERPARATYROIDISM
- Dietary modification + Phosphate
binding drugs
 Calcium acetate
 Calcium carbonate
- ADJUNCT
 Ergocaldiferol: Dose dependent
 Active 1, 25 vitamin D therapy:
calcitriol

Metabolic Action
Stage Description GFR
consequence Plan
5 ESRD (End- <15 • Azotremia • Dialysis
Stage Renal develops or Pre-
Disease) emptive
UREMIA transplant
or palliative
care

8
HYPERTENSION - Obstructive sleep apnea
- Hyper parathyroidism
- Pheochromocytoma
- Primary aldosteronism (increase aldosterone)
- Hyperthyroidism

MEDICATIONS

• Corticosteroids
• Estrogen
• NSAID’s – would inhibit the prostaglandin
production
• Amphetamines- centrally acting agent
• Sibutramine – diet pills
• Cyclosporine
• Tacrolimus- Organ transplantation
o lowers the immune system
• ERYTHROPOETIN -
• Venlafaxine - mental disorders

BARORECEPTOR REFLEX- moment-moment ACC/AHA: AMERICAN COLLEGE OF CARDIOLOGY /

regulation AMERICAN HEART ASSOCIATION– other than JNC 8.

▪ NORMAL- <120mmHg and <80

Low BP- activates SNS
▪ ELEVATED- 120-129 and <80
PERIPHERAL VASCULAR RESISTANCE - pertains to ▪ STAGE I- 130-139 and 80-89
the relaxation and contraction of the blood vessels ▪ STAGE II - >140 and >90
▪ HYPERTENSIVE CRISIS- >80 and >120
BP = PVR x CO
JNC CLASSIFICATION
CARDIAC OUTPUT - pertains to volume of blood being
pump by the heart. ▪ NORMAL - <120 and<80
▪ PRE-HYPERTENSION – 120-139 or 80-89
STROKE VOLUME – this is the volume of the blood ▪ STAGE I- 140-159 or 90-99
being pump by the left ventricle. ▪ STAGE II - >160, >100
VENOUS TONE- this reflects the venous resistance and FACTORS CONTRIBUTING TO HYPERTENSION
pressure.
1. RAAS insulin resistance, hyperinsulinemia
- Strong venous tone, many venous returns. 2. Disturbance in the CNS,
3. Abnormal it in sodium excretion.
VENOUS RETURN- flow of the blood back to the heart.
4. Deficiency to synthesis of vasodilatory
- Many venous returns, increase stroke volume, substance
increase CO, increase MAP a. Prostacyclin – commonly seen on
kidney.
RENIN-ANGIOTENSIN ALDOSTERON SYSTEM- b. Bradykinin – vasodilator and
hormonal feedback loop. bronchoconstrictor
Increased aldosterone – there is Na + H2O. c. Nitric oxide
5. excess synthesis of vasoconstrictor substances -
HYPERTENSION- persistent elevated arterial blood - (angiotensin II- it can activate the
pressure. catecholamine release and at the same time it
can activate the aldosterone. it can also affect
TWO CATEGORIES OR TYPES OF HTN the peripheral vascular resistance and at the
PRIMARY HTN- idiopathic / essential same time it can also affect the cardiac output), -
- (endothelin I)
- Unknown / multi-factorial 6. Dietary: high sodium intake, low calcium intake
- More common. (dairy products)
SECONDARY HTN – known cause

- CKD, Cushing’s syndrome

DIAGNOSIS b. CLONIDINE: It can cause rebound HTN upon
sudden withdrawal
1. ELEVATED BLOOD PRESSURE
2. Fundoscopic examination – there is an arteriolar
narrowing, (increases the pressure). -Treatment: give alpha blocker or reinstitute
3. Cardiopulmonary examination – arrhythmia clonidine
o Left ventricular hypertrophy
4. Lab test: underlying disease o CENTRALLY ACTING AGENTS:
o BUN- blood urea nitrogen / creatinine compensatory response (salt and water
o Lipid profile – atherosclerosis retention)
o Electrolytes – for electrolyte imbalance ▪ Ganglionic blockers:
o Fasting blood sugar – diabetes (hexamethonium, trimethapan)-
o ECG – for the rhythm of the heart. OBSOLETE
o Post ganglionic sympathetic nerve
SECONDARY HYPERTENSION terminal blocker
1. RESERPINE: depletes adrenergic
- Plasma norepinephrine/metanephrine – norepinephrine nerve terminal of the
pheochromocytoma (tumor in the adrenal norepinephrine stores.
medulla wherein it releases adrenaline or 2. GUANETHEDINE, GUANADREL:
epinephrine) deplete and block release of stores
- Aldosterone – hyperaldosteronism OBSOLETE
3. MAO INHIBITORS: cause a
- Renin – captopril stimulation test, renal formation of a false neurotransmitter
angiography (for renovascular disease) (octopamine) in the sympathetic
DRUGS USED FOR HYPERTENSION postganglionic neuronal terminal.

DIURETICS – reduce blood volume] ADRENORECEPTOR BLOCKERS

▪ Thiazide (HCTZ, chlorthalidone) mild- o A1 blocker (prazosin, doxazosin, terazosin)

moderate ▪ Decrease PVR and Venous
o Contraindicated to patient with gout. Return
o It Increases the reabsorption of uric acid - May cause orthostatic HTN/ first dose
in the PCT phenomenon
▪ Loop diuretics (severe to HTN crisis) o Give at bedtime
▪ ADR: electrolyte imbalance - They relax the smooth muscle in the prostate
- low compensatory response is minimal o For Benign Prostatic Hyperplasia (BPH)

SYMPATHOPLEGICS – decrease venous tone, BETA BLOCKERS: initially reduce cardiac output
decrease heart rate, decrease contractile force, - Chronic use: decrease by reducing angiotensin
decrease cardiac output, decrease peripheral level because they can reduce the renin
vascular resistance. release4 from the kidney.
o A2 selective agonist: (clonidine, o Prototype: PROPRANOLOL
methyldopa) o NEBIVOLOL: with vasodilatory action
▪ Decreases sympathomimetic due to nitric oxide release
outflow by activating a3 receptors o Selective (asthma): BEAM (Bisoprolol,
(via negative feedback) Betaxolol, Acebutolol, Metoprolol)
▪ Crosses BBB when given orally VASODILATORS:
- high compensatory response 1. Reduction of calcium influx via L type calcium
a. METHYLDOPA: converted to channel
methylnorepinphrine o Dihydropyridine (amlodipine,
nifedipine)
- DOC for pregnant (with Reno protective o Non-dihydropyridine (verapamil,
property) diltiazem)
2. Release of Nitric Oxide from the drug or the
- may cause hematologic immunotoxicity
vascular endothelium
(false positive Coomb’s test)
o Hydralazine- older vasodilator
- may cause sedation ▪ Systemic Lupus erythematosus
at dose >200mg/day
 o Nitroprusside: mixed vasodilator
▪ Light sensitive, short acting
▪ Used in HTN crisis
3. Hyperpolarization of vascular smooth muscle
through opening of potassium channel
o Minoxidil (for severe HTN)-
compensatory response (tachycardia
and water retention)
▪ Co-administration of Beta-
blockers & diuretic
▪ May cause hirsutism
o Diazoxide: thiazide derived but lacks
diuretic properties
▪ Reduce insulin release and cam
be used for hypoglycemia cause
by insulin producing tumors.
4. Activation of the dopamine 1 receptors
o Fenoldopam- arteriolar vasodilator for
HTN crisis

ACE AND ARBS

ACE (ANGIOTENSIN CONVERTING ENZYMES)

INHIBITORS: ACE, kininase (responsible for the
degradation of the bradykinin), peptidyldipeptidase-> low
aldosterone, ACEII and increase bradykinin

- CONTRAINDICATED: to pregnant may cause

renal damage in the fetus
o Oligohydramnios- low on amniotic fluid
- Useful for patients with diabetes and heart
failure
- TOXICITY: cough, hyperkalemia (can inhibit
aldosterone), angioedema

ARBS: lower incidence

- CONTRAINDICATED: to pregnant
- TOXICITY: hyperkalemia, angioedema

RENIN INHIBITORL: Aliskiren

BARORECEPTOR INHIBITOR: Veratrum viride

alkaloids

- OBSOLETE

NON-PHARMACOLOGIC TREATMENT

1. Reduce sodium intake

2. Lifestyle change
o Exercise
o Decrease fat intake
▪ Decreased weight
o Avoid alcohol
o Avoid stressors
ISCHEMIC HEART DISEASE Myocardial Infarction: Heart attack
- sudden complete blockade of the coronary
Ischemia – lack of oxygen and decreased or no artery
blood flow
Right Coronary artery
IHD: Ischemia in the myocardium (muscle of the
heart)
- commonly cause atherosclerosis
- begins early in life
It may present as: RV LV Left
Acute coronary syndrome (MI) circumflex
Angina artery
- Chronic stable
- Unstable
- Vasospastic angina Right anterior artery

MYOCARDIAL ISCHEMIA
- reduction of coronary blood flow due to stenosis Right Coronary artery: Posterior wall septum and
(abnormal narrowing/hardening of the blood vessel) papillary muscles
- abnormal constriction and dilation of the vessels Blocked: 30-40% MI
- reduced oxygen carrying capacity of the blood.
Left Circumflex artery: Lateral wall of the left
ATHEROSCLEROSIS: most common cause of ventricle
epicardial coronation artery stenosis. 15-25% MI

Left anterior artery: Supply blood to the anterior wall

and septum
40-50% MI

If the artery is blocked—

Example:
1 minute blocked: ischemia
- decrease muscle contraction
- reversible
20-40 minutes: irreversible
- zone of necrosis

If sudden return of blood flow: “sub endocardial

infarct”

PHCP I ISCHEMIA HEART DISEASE JIMENEZ

 Diltiazem: useful for rate control of patients
with Atrial Fibrillation
Verapamil: if patients have obstructive
hypertrophy
Lidocaine: Ventricle arrythmia
Non-ST Elevated MI Calcium Channel blockers: contraindicated in
acute phase MI

ST Elevated MI
STEMI:
Fibrinolytic: Streptokinase
- causes lysis of thrombus if given < 6-12 hrs.

Recombinant Tissue Plasminogen Activator

Alteplase: coverts plasminogen to plasmin
causing lysis
3-6 hours (hindi nabalik yung supply): extension of
ischemia LIPID LOWERING AGENTS:
“Transmural infarct” 1. Statin: HMG-CoA reductase inhibitors
3 Types of CK → 1st line treatment
DIAGNOSTIC TEST: (Creatine Kinase) - reduces intracellular cholesterol
ECG: BB – brain ADR: Rhabdomyolysis
MM – muscle
Cardiac markers: MB – heart Drug Interactions: Azoles, Fibrates and cyclosporin
- CK MB: Creatine Kinase MB 2. Fibrates: Fenofibrate, gemfibrozil
→Primary cardiac marker → PPAR alpha:
→ Increase 3-12 hrs. after the onset of pain (24 ADR: Cholethiasis
hrs.) Bile Acid Sequestrants
→ Baseline (return) after 48-72 hrs. - cholestyramine/ colestipol
Alternative: Colesevelam
Troponin T Niacin: participates in tissue respiration-oxidation
I – specific for heart reaction – decrease LDL and VLDL production
- more specific and sensitive than CK MB - hypertriglyceridemia
- 3-12 hrs., 28-48 hrs. (peak) ADR: Liver toxicity, flushing and itchiness (Aspirin
- return to baseline 5-14 days 325mg before the dose)
Ezetimibe: inhibits intestinal absorption of
Lactate dehydrogenase cholesterol
1 & 2 “Flipped pattern” Omega 3 Fatty Acids:
1>2 = MI
Percutaneous Transluminal Coronary
TREATMENT Angioplasty
1. Stool softeners - PTCA is a treatment for patients with
2. Prophylaxis for stress ulcers coronary artery disease (obstructed
3. Antipyretics blood flow through the coronary
Aspirin/Clopidogrel arteries). The physician inserts a
Oxygen: cyanotic special catheter (a thin, flexible tube)
Beta blockers: IV within 4 hrs. of pain onset into the femoral artery. The catheter
Morphine: (for chest pain) if symptoms are not has a balloon at its tip. X-ray is used
relieved by B-blockers to help the doctor thread the
→ orthostatic hypertension → fainting catheter into position at the site of
ACE Inhibitors + B-blockers: improves the blockage in the coronary artery.
oxygen demand and limit the infarct size

PHCP I ISCHEMIA HEART DISEASE JIMENEZ

Coronary Artery Bypass Graft TYPE OF ANGINA
1. Stable angina
– aka athesclerotic angina
– angina of effort, classic angina
- associated with exertion/ increase oxygen
demand
- Pain is characterized by crushing/squeeze with
radiates to the left arm or left jaw
- relieved by rest
→ Associated with fixed atherosclerotic narrowing.

2. Prinzmetal / Variant angina / Vasospastic /

COMPLICATIONS OF MI Coronary Artery Spasm
• Lethal arrhythmias - aka rest angina
• Heart Failure - 10% cases
• Cardiogenic shock - Reversible spasm
– TREATMENT - Focal deficiency of Nitric oxide
– Vasopressors- NE, epinephrine, dopamine - hyperinsulinemia
– Inotropic drugs- Epi, Dobutamine Isoproterenol, - Low intracellular Magnesium
digoxin - cigarettes smoking
– Vasodilators- Nitroprusside - cocaine use
– Others: intra-aortic balloon pumping 3. UNSTABLE ANGINA
- aka crescendo angina
- characterized by increasing Frequency of Pain.
- Precipitated by progressively Less exertion
- Longer episode than stable angina
- pre infraction angina

4. MICRO VASCULAR ANGINA

- dysfunction of small coronary arteries
- because of carbon monoxide poisoning
- low oxygen
- will lead to carboxyhemoglobin silent ischemia
- unknown etiology
- excessive production of endorphins

COMMON CAUSES:
• Atherosclerosis
• Tachycardia
• Anemia
• Hyperthyroidism
• Arterial hypoxemia
• HypotensioN
Angina: Chest pain
DETERMINANTS OF THE VOLUME OF OXYGEN
REQUIRED BY THE HEART

DIASTOLIC FACTORS
- Blood volume
- Venous tone

PHCP I ISCHEMIA HEART DISEASE JIMENEZ

SYSTOLIC FACTORS muscle relaxation via stimulation of the
- Peripheral resistance dephosphorelation of the myosin light chain
- Heart rate, heart force and ejection time phosphate
- Heart: decrease cardiac size, decrease cardiac
When diastolic and systolic are increased, it will output and preload
result to INCREASED INTRAMYOCARDIAL Short acting:
FIBER TENSION will lead to INCREASE Sublingual (10-20 duration; ISDW: 30 min.
MYOCARDIAL OXYGEN REQUIREMENT duration
Intermediate: Oral 4-6 hours duration
RISK FACTORS: Transdermal: 24 hrs. or more (Tolerance: 8-10
- Gender (more common in women) hrs.)
- increased occurrence with age - remove after 10-12 hours then place again 12 hrs.
- 45 to 64: common in African American after patch free recovery
women ADR: Tachycardia, orthostatic HTN
- 65 to 74: common in African American - Throbbing headache/ Monday
men
CALCIUM CHANNEL BLOCKERS
DIAGNOSTIC TESTS: - Verapamil/ Diltiazem: block the calcium
dependent conduction of the AV nodes:→ can be
1. 12 LEAD ECG used for AV Nadal arrhythmia
- 50% stable angina or more (normal) in - Prophylaxis for stable and variant angina
stable angina
- ST-T wave consistent with myocardial DIHYDROPYRIDINE: evoke greater vasodilation
ischemia - May result to sympathetic reflex and
- Q waves from previous MI increase H.R
- St segment elevation/depression ADR: Constipation, pretibial edema, nausea
flushing, dizziness
2. STRESS TESTING: For patients who can Verapamil: AV blockade, and sinus node
tolerate exercise depression
POSITIVE TEST: Less than or equal to 1mm
ST segment depression/elevation for 60-80 BETABLOCKER: Prophylaxis for stable angina
seconds either during or after the exercise. - Avoid in vasospastic angina
- Caution in patients with Diabetes Mellitus:
3. STRESS PERFUSION IMAGING may mask symptom of hypoglycemia
- Thallium 201 (Tachycardia)
- reserved for patients with ECG abnormality
- can also diagnose multi –vessel disease/localized BETABLOCKER/
COMBINATIO
CALCIUM
ischemia NITRATES N OF BB + N
CHANNEL
or CCB + N
BLOCKER

4. CORONARY ANIOGRAPHY & CARDIAC HEART RATE Reflex increase Decrease Decrease

CATHETERIZATION ARTERIAL
Decrease Decrease Decrease
- specific and sensitive but this is invasive, risky PRESSURE

and expensive. END DIASTOLIC

Decrease Increase Decrease
PRESSURE

No change/
TREATMENTS CONTRACTILITY Reflex increase Decrease
decrease

EJECTION TIME Reflex decrease Increase No change

ASPIRIN: 80-100mg enteric coated (for stable
angina) NET
MYOCARDIAL
Decrease Decrease Decrease
Alternative: Clopidogrel OXYGEN
REQUIREMENT

NITROGLYCERIN: Nitric oxide → stimulates the

guanylyl syclase → CGMP and causes smooth

PHCP I ISCHEMIA HEART DISEASE JIMENEZ

NEW DRUGS

Ranolazine: reduces the late prolonged sodium

current at the myocardial.
Ivabradine: inhibits the If sodium current in SA
Nodes
→ hyperpolarization → Decrease heart rate →
decrease cardiac work
Trimetazidine: inhibits fatty acid oxide → improves
myocardial glucose utilization.

-------------------------------END-------------------------------

PHCP I ISCHEMIA HEART DISEASE JIMENEZ

PHCP FINALS Afferent arteriole
- Entrance of the blood
ACUTE KIDNEY INJURY - Then it will be blood will be filtered to the
Kidney glomerulus
- A pair of bean shaped organs located below the
ribs and belly Efferent arteriole
- Uses: - Exit of the blood
1. Removes waste and excess fluid - Lalabas ang filtrate (waste)
2. Removes drugs from the body
3. Balances body’s fluid and electrolytes Bowman’s capsule
4. Releases renin and regulates BP - Filtrate entrance
5. Produces calcitriol, an active form of Vit D - Entities that can enter:
6. Produces erythropoetin for RBC o H2O
production o Glucose
Nephron o Amino acid
- Functional unit of kidney o Inorganic ions (Na, Cl, K, HCO3)
- 1,000,000 per kidney o Wastes (Creatinine, Urea)

URINARY TRACT Proximal convoluted tubule

- Diuretics: Carbonic anhydrase
- % that can be absorbed:
o H2O – 65%
o Glucose – 100%
o Amino acid – 100%
o Inorganic ions
 Na – 65%
Deoxygenated blood → vena cava paangat sa portal  Cl – 65%
area sa bandang liver papunta sa heart  K – 65%
 HCO3 – 90%
Oxygenated blood → aorta to renal artery and vein o Wastes
don papasok and lalabas ang dugo  Creatinine
 Urea – 50%
Kidney filters blood, ang nalinis na dugo (filtered)
- Whatever is not being excreted is reabsorbed.
babalik sa systemic circulation. The filtrates ay
Or else, the creatinine and urea will go back to
mapupunta sa ureter going to the bladder as a form of
the systemic circulation
urine and dadaan sa urethra and maeexcrete na sa body
via MICTURATION (urination)
Descending and Ascending Loop of Henle
Medulla – salty part of the urine
- Diuretics: Loop
- Half of it is dipped to medulla (salty)
NEPHRON DIAGRAM
- As the filtrate goes down the water is
reabsorbed, the salt is not.
- Impermeable to salt
- As it goes down it is concentrated
- H2O to the left is reabsorbed
- Na to the right in the medulla and it makes it
salty

Distal Convoluted tubule

- Diuretics: Thiazide
- 25 % of remaining Na is reabsorbed
- Aldosterone will open a pore to have exchange
of ions (Na-out; K-in)

1
Collecting duct Intra-renal:
- Diuretics: K sparing diuretics 1. Acute glomerulonephritis
o it inhibits the excretion of K - Inflammation of the glomerulus
- Vasopressin is anti-diuretic hormone - Can be infection (S. pyogenes) or SLE
o It will open pores in the collecting duct, 2. Acute tubular necrosis
habang bumababa, ang filtrate - 50% of the intra-renal
bumabalik - The cells in the tubules are damaged
- High ADH means dehydrated 3. Acute interstitial nephritis
- Spaces between the tubules become
Creatinine, by product of muscle (muscle waste). High inflamed causing decrease kidney capacity to
serum creatinine & high urea (Blood urea nitrogen) filter properly
means a kidney problem. - Vasoconstriction lead to obstruction
- Urine can’t pass because of the obstruction
Acute renal failure - Can cause backflow of urine
- Sudden, reversible decrease in GFR (glomerular
filtration rate) DRUGS THAT IS TOXIC TO KIDNEY
- Characterized by: 1. NSAIDs
1. Increase in serum creatinine of about 0.3 - Inhibits prostaglandin production
mg/dl. Normal values: (vasodilator)
o Male (0.9-1.3 mg/dl) - Also a renal vasodilator in the afferent
o Female (0.6-1.1 mg/dl) tubule, if we don’t have vasodilatory action in
2. Increase in serum creatinine of 50% the afferent it will be constricted and the
greater than the baseline renal blood flow will decrease and will cause
3. Reduction in urine output (0.5ml/kl) for 6 low GFR and can cause kidney damage.
hours - Limits afferent arteriole vasodilation
o Polyuria – plenty
o Anuria – none 2. ACE inhibitor
o Oliguria – decrease urine output - Best medication for HTN in the CKD
- Contraindicated for AKI
3 TYPES OF ACUTE RENAL FAILURE - Limits renal efferent constriction
1. Pre renal - Efferent constriction is needed to maintain
- Before the kidney GFR due to lower renal perfusion
- There is severe decrease in BP/ there is flow
obstruction 3. Aminoglycosides
- Atherosclerosis - Accumulate in the renal cortex
- Ischemia - AKI present within 5-7 days of discontinuation
- When left untreated can damage the kidney - Hypomagnesia is common
2. Intra renal
- in the kidney 4. Contrast Media
- direct damage - Galodinium – MRI
- inflammation - Oral Sodium Phosphate
- infection 1. Hypoxia in the renal medulla
- drugs 2. ROS (radioactive oxygen species)
- autoimmune (SLE) 3. Tubule obstruction with precipitated
- When left untreated can lead to CKD contrast material
3. Post renal
- After the kidney 5. Amphotericin B
- Obstruction of urine flow - ROS
- BPH - Dose and duration dependent
- Kidney stones
- Cancer / tumor 6. Acyclovir
- When left untreated can damage the kidney - Precipitates in tubules
- Obstruction when given 500mg/m2 IV bolus
2
7. Antibiotics TOXIN THAT OUR BODY PRODUCES
- Acute interstitial nephritis 1. Myoglobin
- Released by injury muscle cells
8. Chemo (Cisplatin & Carboplatin) 2. Hemoglobin
- Accumulation in PCT which cause necrosis - Due to massive hemolysis
and apoptosis - Pigment nephropathy
3. Rhabdomyolysis
9. Ifosamide
- Fanconi’s syndrome (as well as tetracycline) Isosthenuria
- Failure to concentrate / dilute urine
10. Bevacizumab - Diagnostic factor
- Proteinuria o Pre-renal
- Bawal and protein sa urine because if that is a  > 500 mOsm/kg urine Osmolarity
macromolecure hindi makakalagpas sa o Intra-real damage
bowman’s capsule. If amino acid,  > 300 mOsm/kg urine Osmolarity
marereabsorb sa PCT. If Albumin, is negative
charge and kidney also is a negative charge RECOVERY FROM AKI
therefore if both negative leads to repelling 1. Pre-renal – restore GFR
action. 2. Intra-renal – restore GFR, remove toxin, initiate
- How to know there is proteinuria? therapy
Microscopic if turbid or puss. 3. Post-renal – recovery depends on the size of the
- How to know there is blood in urine? Cola functioning nephron
colored or brown urine.
- How to know there is glucosuria? DIAGNOSTCIS
Nilalanggam, sign of diabetes. 1. Angiography
- Cannot be in urine: 2. Renal biopsy
o Protein 3. Urinalysis
o Albumin - Presence of RBC:
o Ketone o Eumorphic: collecting system
o Sugar o Dysmorphic: glomerulonephritis
o Blood - Presence of WBC:
o Pyelonephritis
11. Mitomicin & Gemctabine o Acute interstitial nephritis
- Thrombotic micropathy - Presence of Uric acid:
o Ethylene glycol poisoning
TOXIC INGESTIONS o Calcium oxalate crystals
1. Ethylene glycol 4. Bladder Pressure
- Automobile antifreeze - >25 mmHg
- Can cause tubular injury - Abdominal compartment syndrome
o Oxalic acid - AKI
o Glycoaldehyde 5. Biomarkers
o Glyoxylate - NGAL: neutrophil gelatinase associated
2. Diethylene glycol lipolactin
- 2 hydroxy ethoxy acetic acid - Serum cystatin C
3. Melamine 6. Ultrasound
- Infant formulation - Doppler echography
- High proteins - For thromboembolic / renovascular disease
- Can cause nephrolithiasis obstruction 7. Nuclear scanning
4. Aristocholic acid - TC-99 MAG 3: Technitium 99 Mercaptoacetyl
- “Chinese herb nephropathy” triglycerin
- Balkan nephropathy - TC-99 DTPA: Technitium 99 Diethylene
triaminepentaacticacid
- Iodine 131
3
MANAGEMENT
1. Correct fluid overload/edema
- Furosemide IV – minutes (onset)
- Furosemide Oral – hours
- Contraindicated: Aminoglycosides & NSAID
2. Correct acidosis (bicarbonate)
3. Correct hyperkalemia
- Decrease K intake
- Give potassium binding resin
- Sodium polystyrene sulfonate
- Promote K intracellular shift:
o Insulin
o b-agonist
o dextrose solution
4. Correct hematologic deficiencies
- Transfusion, estorgen, desmospressin
5. Correct hyperphosphatemia
- Give IV calcium: chelation
- Oral calcium: binds to phosphate in the gut
- Sevelamir: non-ionic polymer that binds to
phosphate in the gut
- Aluminum hydroxide
- Dialysis
6. For hypocalcemia
- Calcium gluconate
7. For hyponatermia
- Fluid restriction
- NaCl – slow IV to avoid pulmonary edema
8. Avoid nephrotoxic drugs
- N-acetylcysteine for contrast media
- Give vasodilators: Fenoldopam
- Give CCBs: Nifedipine

(140 − 𝑎𝑔𝑒) × 𝑘𝑔
𝐶𝑟𝐶𝑙 𝑚𝑎𝑙𝑒 =
73 (𝑠𝑒𝑟𝑢𝑚 𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒)
𝐶𝑟𝐶𝑙 𝑓𝑒𝑚𝑎𝑙𝑒 = (𝐶𝑟𝐶𝑙 𝑚𝑎𝑙𝑒) × 0.85

*Mas konti ang muscle mass ng female

4
CHRONIC KIDNEY DISEASE (CKD) HYPERTENSION:
Thickening of Afferent Arteriole
- Chronic renal failure
↓
- Pathological abnormality of the kidney
Decrease Renal Blood Floe
- Characterized by:
↓
o Hematuria
Decrease Filtration
o Proteinuria
↓
o Reduction of GFR / Creatinine clearance
Decrease GFR (kidney will produce renin)
≤ 60 ml/min
↓
- Irreversible
Activation of RAAS
↓
Causes of CKD:
Increase Heart Rate and Blood Pressure
1. Acutre renal failure
2. HTN - 2nd most cause
Notes:
3. Diabetes – most common cause
Chronic Activation of RAAS and thickening of AA would
- Diabetic nephropathy
cause damage to nephron and lead to glomerulo
4. Kidney disease
sclerosis (scar inside), there would be ischemia (loss of
- Cancer, obstruction
oxygenation).There is healing in portion but loss of
function.
ACUTE RENAL FAILURE
Pre renal Chronic: Glomerulosclerosis → Ischemia → death of
- Can cause renal artery stenosis (hardening) nephron
o No more contraction and dilation
- Heart failure HTN
- Hemmorhage - Loss of nephron
Which cause decrease the flow of blood going to the - Glomerular hyperfiltration lead to overworks
kidney ↓
↓ Sclerosis
Intra renal → CKD ↓
- Glomerulonephritis Too much death
- Acute tubular necrosis ↓
- Acute interstitial nephritis Decrease GFR
↑ ↓
Post renal Retention of waste
- BPH ↓
- Renal stone Toxic to the body
- Tumors
DIABETES
AKI/ARF CKD High blood sugar → ROS (free radicals)
↑ SC 0.3 mg/dl Hematuria ROS → activates growth factor
↑ SC 50% of baseline Proteinuria (Cytokines & oxidative stress)
Urine output < 0.5 GFR < 60 ml/min ↓
ml/kg/h for 6 hours Diabetic nephropathy
(changes in the nephron)
- hours to weeks - long standing
- reversible - irriversible
- can be CKD if left
untreated

5
 Loss of nephron = ↓calcitriol → ↓ ca reabsorption (GIT,
Kidney) → Hypokalemia → hyperparathyroidism →
breakdown of bones (bone resorption) →
OSTEODYSTROPY (nagiging weak ang bones)

Loss of nephron = ↓ GFR, other ions is not excretes

including PHOSPHATE
Thereby, ↑ phosphate it would activate parathyroid
hormone to have bone resorption
(HYPERPHOSPHATEMIA)

UREMIA
- Retention of nitrogenous waste in the blood
- AZOTEMIA (not severe) → Uremia
DIABETIC NEPHROPATHY - What would happen when there is uremia
1. Mesangial expansion o Neurologic problem
- Cannot filter well o Anorexia, vomiting
Mesangium o ↓of estrogen → amenorrhea
- Removes the trap residues of protein para o ↓ testosterone → impotence
kapag nagfifilter ang glomerulus maayos pa din o Skin changes (rashes)
- Keeping the filter free from debris - In the later sage
2. Podocytopathy o ↓renin → ↓ BP
o ↓EPO anemia → anemia
- Podocytes
o ↓ calcitriol → renal osteodystrophy
o Prevents protein from entering the
nephrons
3. Glomerular Basement thickening STAGES OF CKD
- Inflammation and scarring Stage GFR/ CrCl (ml/min)
- Can lead to nephron death 0 > 90
1 ≥ 90
CLINICAL MANIFESTATION 2 60-89
1. Na and H2O balance 3 30-59
- Dec GFR = Na & H2O retention → HTN → 4 15-29
Peripheral edema 5 (End-Stage
- Restrict fluid intake < 15
Renal Disease)
2. Potassium balance
- Dec GRF = increase K retention → (140 − 𝑎𝑔𝑒) × 𝑘𝑔
Hyperkalemia 𝐶𝑟𝐶𝑙 𝑚𝑎𝑙𝑒 =
73 (𝑠𝑒𝑟𝑢𝑚 𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒)
- Muscle weakness, arrhythmia (140 − 𝑎𝑔𝑒) × 𝑘𝑔
𝐶𝑟𝐶𝑙 𝑓𝑒𝑚𝑎𝑙𝑒 = × 0.85
- Loss of nephron = ↓renin production = 73 (𝑠𝑒𝑟𝑢𝑚 𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒)
↓aldosterone → DCT will not work → K RISK FACTORS
retention 1. age > 50 y/o
- DO NOT USE K SPARING DIURETICS & ACE 2. HTN
INHIBTOR 3. Male gender
3. Metabolic acidosis 4. African American / Hispanic race
- ↓ capacity to excrete H ions and generate 5. Family history
bicarbonate → acidosis 6. Smoking
7. Obesity
- Acidosis leads to bone decalcification
8. Long term analgesics (NSAIDS)
4. Kidney
9. Diabetes
- Release renin, erythropoietin, calcitriol 10. Auto immune disease

6
COMMON SIGNS & SYMPTOMS - STATINS: additional therapy: has
1. Fatigue cardioprotective effect in px with CKD and
2. Anemia → dec EPO in < 50 ml/min cardiovascular disease.
3. Edema – Na & H2O retention o GOAL: LDL <70mg dL
4. Nausea & pruritus – accumulation of waste product o Non-dihydropine CCBs
5. Infection  For patient experiencing cough,
6. Arthralgia – masakit ang joints angioedema, hemodynamic decline
of renal function and hypokalemia
OTHER DIAGNOSTIC FACTORS  Has more proteinuric-lowering effect
1. BPH than other antihypertensive agents
2. Foaming appearing urine (protein) o STATINS: additional theraoy for cardio
3. Cola color urine protection
4. Rashses - Adjunct therapy
o If the target BP is not achieved with the
use of non-dihydropyridine CCB
CLINICAL INDICATOR
o HCTZ: maximum of 50 mg/day
1. Microalbuminuria
o Atenolol: max. of 25-50 mg/day
2. Proteinuria > 300 mg//day
o Metoprolol: max. of 100 mg.day
3. Hematuria
o SECONDARY OPTIONS:
 Aliskiren – renin inh
STAGES OF RENAL DYSFUCTION  Hydralazine – vasodilator
Metabolic Action
Stage Description GFR  Minoxidil – vasodiator
consequence Plan
1 Normal or ↑ >90 At ↑ risk of CKD: 1. Screen  Clonidine – a2 agonist
GFR- people 1. HTN for CKD
with ↑ risk or 2. Diabetes risk Metabolic
Stage Description GFR Action Plan
with early 3. Obesity 2. Establish consequence
renal damage diagnosis 3 Moderate 30- • Decreased • Monitor
3. Treat renal failure 59 calcium GFR monthly
underlying (CRF) absorption • Avoid
diseases (GFR <50) nephrotoxic
4. Retard • Lipoprotein drugs
progression activity falls • Prescribe
2 Early renal 60- Concentration of 1. Control • Malnutrition antiprotenuric
insufficiency 90 parathyroid BP • Onset of drugs
hormone starts 2. Control anemia (↓EPO) •ACEI or
to rise DM ARBs
3. • Adjust drug
Protenuria dose
reduction
STAGE 3
Treatment:  Identidy co morbidities such as anemia and
For stage 1 and 2 WITHOUT UREMIA: secondary hyperparathyroidism
- ACE inhibitor / ARBS  Anemia maybe treated with erythropoietin
o If px has proteinuria > 500mg/day: reduce replacement if Hb falls to <1-g/dL
BP to <125/75 mmHg and proteinuria to < o Target Hb: 11-12g/dl
500 mg/day  Hyperparathyroidism, calcium phosphorus levels
o ACEI and ARBS are the first line treatment should be intact
for controlling BP to a goal and proteinuria o Dietary restriction and/or phosphate
is < 500mg/day, control BP to a goal of binding medications
<130/80mmHg
- Both drugs are associated with hyperkalemia in
patients with acute renal failure, this is
reversible once medication has been
discontinued.

7
 Metabolic STAGE 5 with UREMIA
Stage Description GFR Action Plan
consequence  First line: Dialysis
4 Severe renal 15- • Triglyceride • - Renal replacement therapy is initiated once
failure (Pre- 29 concentrations Preparation
End stage start to rise for renal patient has stage 5 and or signs of uremia
renal failure) • Hyper replacement o Weight loss
phosphatemia therapy o Lack of appetite
• Metabolic o Nausea
acidosis o Acidosis
• Tendency to o Hyperkalemia
produce
hyperkalemia - Peritoneal dialysis: peritoneal catheter is
inserted in the abdomen
STAGE 4 - Haemodialysis: prescribed 3 times a week for 4
 Educate px about renal replacement therapy hours each session
such as dialysis and kidney transplantation  Second line: Kidney transplantation
 Kidney transplantation is recommended once
GFR falls under <20mL/min Treatment for the underlying risk factors:
 Parathyroid hormone with active vitamin D3  Glycemic control
must be maintained at 70-110 nanograms/L  Goal of BP: <130/80 mmHg with ACEI/ARBs
 <125/75 for patients with proteinuria >
TREATMENT FOR STAGE 3 500mg/day
 ACEI/ ARBS  Tobacco cessation
 STATINS  Protein restriction in stages 4 & 5
 ADJUNCT
 NOTE: ALISKREN + ACEI/ARBS is FOLLOW UP RECOMMENDATION
contraindicated to patients with diabetes Monitoring
because of the risk of renal impairment, - Annual evaluation of serum creatinine
hypotension, hyperkalemia - Estimation of GFR
 Avoid also in patients with moderate to severe - For Established CKD
renal impairment. - Rate of progression should be serially assessed
 Patients with ANEMIA starting Stage 3
- ADJUNCT: recombinant erythropoietin - Screening anemia and bone mineral disorders at
therapy least every 6 months
 Erytropoeitin Alfa - Annual lipid profile
 Patients with SECONDARY
HYPERPARATYROIDISM
- Dietary modification + Phosphate
binding drugs
 Calcium acetate
 Calcium carbonate
- ADJUNCT
 Ergocaldiferol: Dose dependent
 Active 1, 25 vitamin D therapy:
calcitriol

Metabolic Action
Stage Description GFR
consequence Plan
5 ESRD (End- <15 • Azotremia • Dialysis
Stage Renal develops or Pre-
Disease) emptive
UREMIA transplant
or palliative
care

8
CONGESTIVE HEART DISEASE/CONHESTIVE HEART • AFTERLOAD: force or load against which the heart has
FAILURE to contract to get the blood.
→ eject
Deoxygenated blood – blue – vein except for pulmonary
• STROKE VOLUME: amount of blood pumped out of
vein (which carries oxygenated) the heart from the left ventricle
Oxygenated blood – red – arteries – except for
pulmonary artery (which carries deoxygenated blood) • TOTAL VOLUME: total amount of blood in the
chamber (lahat ng napupunta sa left ventricle)

• EJECTION FRACTION: percentage of how much blood

the LV pumps out to the aorta with each contraction
EF = Stroke Volume / Total volume x 100
EF = 400 mL/100 mL x 100 = 40% EF

MYOCYTES - is the type of cell found in some types of muscle tissue.

FRANK STARLING MECHANISM

Deoxygenated blood from Upper extremities → • Inc stroke volume, if there is increase in left
Superior vena cava → ventricular volume due to myocyte stretch
Lower extremities → inferior vena cava causing a more forceful contraction

VC → Right atrium → Right ventricle → Pulmonary

artery → Lungs ➔ oxygenation ➔ travel back to the
heart → pulmonary vein → Left atrium → Left ventricle
→ Aorta → systemic circulation → oxygen ------- vena • Greater recoil → inc. stroke volume (amount of
cava blood pumped out by the heart)
• Frank starling mechanism has a limit because
muscles get tired and eventually it may cause
damage.

• Compensated heart failure

– If the dilated veins are able to meet the
cardiac output requirement
-- Frank starling mechanism is still effective

• Decompensated heart failure:

– Increasing dilation → inc. ventricular wall
Tension → inc. oxygen demand
– Failure to meet the need for demand even at rest.
Left ventricle → large muscle → it pumps OXYGENATED
blood to aorta to systemic circ.

HEART FAILURE: Inability of the heart to pump blood at

rate that meets the requirement

• PRELOAD: Initial stretching of the myocytes prior to

contraction
Before ma pump to aorta
→ PRE
Systolic HF Diastolic HF - Hypertrophic Cardiomyopathy → genetically induced
Due to inability of Blood build up The left ventricle is increase in thickness of the LV → Concentric.
the heart to because pump not filling enough. - Restrictive cardiomyopathy → stiffness of the muscles
pump hard is not enough to It may either be of the LV → no stretching and less filling → Diastolic HF
enough supply blood → presented via
→ Build-up in LV Back flow of reduced preload Congested heart → decreased renal blood flow →
→ back flows to blood to the (but normal activation of RAAS → Fluid retention → Inc. BP → Back
Pulmonary vein lungs/systemic ejection fraction) flow to the lungs → Inc respiratory pressure →
→ Lungs circulation. → In cases of Pulmonary edema → Dyspnea → Orthopnea (when
How to know if hypertrophy – laying down feels like drowning naaks)
may Systolic HF? lumiliit yung space Crackles → tubig sa lungs
➔Ejection ng chamber to hold
fraction (percentage SYSTOLIC HF → blood RSHF
of how much blood the DIASTOLIC HF TV: 80 → backflow to jugular vein (jugular vein distension)
LV pumps out to the
aorta with each
→ dangerous SV: 40 → blood will backflow to liver and spleen (causing
contraction) Normal ejection
hepatosplenomegaly → cirrhosis (fluid itatapon sa
Dapat if 100 mL fraction
yung TV, 100 mL peritoneal cavity) → Ascites
But because of
din yung ma- inflamed? Ventricle → Blood will backflow to the interstitial space of the
pump out → konti nalang legs → fitting edema
yung nafifill = Arrhythmia because
sira yung pag pump →
Notes: cause irregular pumping
Ejection fraction normal: 50-70% comfortable during
activity
Borderline HF:41-49% symptoms during activity
Reduced: <40%: symptoms become noticeable even at
rest
Myocardial structural changes
Left sided HF: Common || Back flow sa lungs • Hypertrophy: to increase the mass of the contractile
Right sided HF || Back flow sa systemic circ. tissue since cardiac myocytes cannot proliferate.
Both sides: Biventricular HF || Backflow in both lungs
• Increased diameter of individual muscle fibers
and systemic circ.
Right sided can become Left sided HF – Concentric hypertrophy: thickness of the wall
increases without increase in size of the chamber
– Eccentric hypertrophy: thickness of the wall and size
WHAT CONTRIBUTES TO HEART FAILURE?
of the chamber both increases to accommodate
- Existing heart failure
preload
- Chronic HTN → Inc. Arterial pressure → there would
be difficulty of LV to pump blood → frank starling
mechanism (mag dou-double time) → hypertrophy →
Inc. O2 demand
* coronary arteries may also be affected or squeezed →
dec. supply of blood → dec. oxygen supply

Inc O2 demand + O2 supply = Weaker contraction

- Dilated Cardiomyopathy → Chamber dilates to
accommodate preload.
→ there is dilation of LV to accommodate preload →
stretching of muscle walls → eventually, thinning of the
wall → systolic heart failure Clinical features
- Diastolic Heart Failure → hypertrophy of the LV ✓ Dyspnea
causing dec. chamber size – Due to fluid transudation into air spaces
 ✓ Orthopnia ✓ Oliguria
– Due to increased venous return from the – Late finding in heart failure and is found in
lower extremities and by elevation of the patients with markedly reduced cardiac
diaphragm in the supine position. output from reduced LV function.
✓ Paroxysmal nocturnal dyspnea
– Breathenessness awakening patients during - Limited fluid at 1 L a day
asleep due to extreme dyspnea bordering on
suffocation. Clinical Presentation of HF
- habang natutulog Symptoms Signs
✓ Orthopnea • Dyspnea, particularly • Pulmonary rales
• Dec. pooling of the blood in the lower on exertion “crackles”
Extremities → shifting of blood from the • Orthopnea • Pulmonary edema “inc
extra thoracic to the thoracic • Paroxysmal nocturnal pressure in lungs”
• Since the LV is failing → the blood is not dyspnea • S3 gallop “lub dub ta”
pumped out easily without having to • Exercise intolerance • Cool extremities
dilate → increase in pulmonary pressure
• Tachypnea • Pleural effusion
→ inc. pulmonary edema → dec. pulmonary
compliance → increase in airway resistance → Dyspnea • Cough • Cheyne-Stokes
✓ Paroxysmal Nocturnal Dyspnea • Fatigue – dyspnea and irreg Respiration “irregular
• Occurs at night breathing breathing”
• Sudden awakening of the patient after a couple of • Nocturia • Tachycardia
hours of sleep with a feeling of severe anxiety, • Hemoptysis • Narrow pulse
breathlessness and suffocation. • Abdominal pain pressure
• P.N.Dyspnea VS orthopnea • Anorexia • Cardiomegaly
– PND may require 30 minutes or longer in • Nausea “overworked heart”
sitting position to feel relief • Bloating • Peripheral edema
– Orthopnea could be relieved faster • Poor appetite, early • Jugular venous
✓ Pulmonary Edema satiety distension
– Sudden increase in Pulmonary Capillary • Ascites • Hepatojugular reflux
Wedge Pressure (PCWP)- usually more than • Mental status changes • Hepatomegaly
25mm Hg
✓ Chest Pain
– May result from myocardial Ischemia from Laboratory Tests
coronary disease or secondary myocardial
ischemia from increase filling pressure or poor
• BNP > 100 pg/mL
cardiac output, hypotension or hypoxemia
– B-type natriuretic peptide (BNP)
✓ Palpitation:
Inc BNP – mas need umihi
– May be secondary to sinus tachycardia due
• Serum creatinine may be increased
to decompensated heart failure, more
because of hypoperfusion. Preexisting renal
commonly in tachyarrhythmia
dysfunction can contribute to volume
- compensatory mechanism
overload.
✓ Nocturia
• Complete blood count useful to determine if
– Recumbency reduces the deficit in
heart failure is a result of reduced oxygen carrying
cardiac output in relation to oxygen
capacity
demand and renal vasoconstriction
• Chest radiography is useful for detection of
diminishes and urine formation increases.
cardiac enlargement, pulmonary edema,
and pleural effusions *opaque
• Hyponatremia, serum sodium <130 mEq/L, is Treatment goals
associated with reduced survival and may
The goals of therapy in management of chronic heart
indicate worsening volume overload and/or
failure are to:
disease progression
• improve the patient’s quality of life;
• relieve or reduce symptoms;
Basic lab test • prevent or minimize hospitalizations for
• CBC- may indicate anemia or infection as potential exacerbations of heart failure;
cause of HF • slow progression of the disease process;
• Urinalysis- may reveal protenuria which is associated • and prolong survival
with CVD
• Electrolytes- may cause fluid retention and renal Diuretics
dysfunction
• To antagonize the compensatory mechanisms of HF
• BUN- may indicated decreased renal blood flow
which is fluid retention often leading to pulmonary and
• FBS- diabetes significantly increase risk of HF
systemic congestion.
• Liver function test- may indicate liver dysfunction due
• Most rapid in producing symptomatic benefits.
to HF
• Though does not alter disease progression or prolong
• B-type natriuretic peptide and Non- terminal pro-B
survival. *
type- increased in HF and are closely corelated with
• Thus, if there is no fluid retention, there is no need for
the HNYA classification.
diuretic therapy.
• ECG- 12-lead- May reveal arrhythmia, ischemia/
infarction and CAD as possible cause of HF
Benefits:
• Improve state of fluid retention,
• improve exercise tolerance,
• quality of life,
• and reduce hospitalizations from heart failure
• Diuretics accomplish this by decreasing pulmonary
and peripheral edema through reduction of preload.
• Though a reduction in preload improves symptoms, it
has little effect on the patient’s stroke volume or
cardiac output.

NY HAFC Thiazides
Class I – mild • Infrequently used alone.
Class II – physical activities but SOB • Preferred in patients with mild fluid retention
Class III – Comfortable at rest but physical activity may
be limited * mark limitations Loop Diuretics
Class IV – even at rest • Good for maintaining euvolemia

TREATMENT ACE inhibitors

• 5D’s*
• Considered as the cornerstone of pharmacotherapy
– DET
– DIURETIC for patients with heart failure.
– DILATORS • Decreases angiotensin II and aldosterone which
– DIGITALIS would attenuate many of the deleterious effects of
– DILATREND- carvedilol
these neurohormones. *
• Oxygen
*Beta blockers: Metoprolol or Carvedilol
• Improves survival by 20-30%
• The most common cause of heart failure is ischemic Digoxin
heart disease*
• Have been in clinical use for more than 200 years
• Where MI results in loss of myocytes, followed by
though only during the 1980s did a study proved its
ventricular dilation and remodeling.
clinical use.
• Studies indicate that ACE inhibitors after MI improve
• A positive inotropic drug, it should be used only in
overall survival, decrease development of severe heart
patients with below normal LVEF.
failure, and reduce reinfect ion and heart failure
• It was shown to reduce morbidity in patients with HF,
hospitalization rates.
providing important symptomatic relief, though it does
• ACE inhibitors also are effective for preventing the
not improve survival in HF patients.
development of heart failure and reducing
cardiovascular risk.
Enalapril
• Decreases the risk of hospitalization for
worsening heart failure
• Similar to patients with concomitant DM
• Even in atherosclerotic diseases, ACEi
reduce development of stroke, MI

Beta blockers
• Proven overwhelmingly by various studies that
they reduce morbidity and mortality.
• Studies were done on large populations using
placebos. Almost all those studies were stopped
prematurely due to overwhelming reduction in
mortality (35-65% Carvedilol, Metoprolol)
• Metoprolol CR/XL, carvedilol, and bisoprolol
are the only β-blockers shown to reduce mortality in
large heart failure trials.
• Though the mechanism by which β- blockers exert
their therapeutic benefit is unclear. *
• Though it is clear that β-Blockers would antagonize
the detrimental effects of the SNS
• Potential mechanisms to explain the favorable
effects of β-blockers in heart failure include:
• antiarrhythmic effects, *
• attenuating or reversing ventricular remodeling,
• improving left ventricular systolic function*, Carvedilol, Bisoprolol, Metoprolol → chronic stable failure
Natriuretic peptide → inc releasse of sodium
• decreasing heart rate and ventricular wall stress
Class I pwede pa mag exercise || II, III, IV restrict exercise. All
thereby reducing myocardial oxygen demand,
stages → salt restriction
• and inhibiting plasma renin release. *
Long term use can inhibit release of renin
OUR LADY OF FATIMA UNIVERSITY
COLLEGE OF PHARMACY

Autonomic Nervous System

Disorders:
Glaucoma
CLINICAL PHARMACY AND
PHARMACOTHERAPEUTICS
PHCP311
 OUR LADY OF FATIMA UNIVERSITY
COLLEGE OF PHARMACY

Objectives:
•  To explain the pathophysiology of Autonomic
Nervous System Disorders
•  To identify factors that may induce and potentiate
the disorders
•  To discuss the clinical presentation as well as the
diagnosis and laboratory evaluation
•  To create a therapeutic outcome

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Glaucoma
•  refers to a collection of diseases characterized
by distinctive changes in the visual field and in
the cup of the optic nerve.
–  Most are associated with elevated intraocular
pressure, although some individuals with normal
intraocular pressure may develop characteristic
optic nerve and visual field changes (normal or
low-tension glaucoma).

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311
OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311
 Intraocular Pressure

Parasympathetic simulation Sympathetic stimulation

(Decreases intraocular pressure) (Increases intraocular pressure)
Ciliary muscle contraction Ciliary muscle relaxation
Pupillary sphincter muscle Pupillary dilator muscle
contraction (miosis) contraction (mydriasis)
Opens trabecular meshwork – Blocks trabecular meshwork –
promotes fluid drainage increases pressure

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Glaucoma
•  Open-angle •  Angle-Closure
–  Aqueous humor has –  Peripheral zone of the iris
complete access to the adheres to the trabecular
trabecular meshwork meshwork and physically
–  Elevation in IOP results impeded the egress of
from an increased aqueous humor from the
resistance to aqueous eye
outflow in the open angle –  With intermittent
–  Slowly progressive, usually prodromal symptoms:
asymptomatic until onset •  Blurred vision with halos
of substantial visual field around lights, headache
loss –  Acute episodes
–  Central visual acuity is •  Cloudy, edematous cornea,
maintained ocular pain, NV, abdominal
pain, diaphoresis

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Angle-Closure Glaucoma
•  Iris apposition blocks passage of aqueous humor from
posterior to anterior chamber
•  Pressure builds in posterior bowing the iris forward

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Angle-Closure Glaucoma
•  Signs and symptoms
–  Acute loss of vision
–  Narrowing of anterior
chamber angle
–  Severe pain
–  Photophobia
–  Blurred vision
–  Red eye with a steamy
cornea
–  Pupil fixed and
nonreactive to light

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Angle-Closure Glaucoma
•  Clinical Interventions
–  Pilocarpine w/ systemic carbonic anhydrase
inhibitor to quickly lower pressure
–  Laser surgery

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Neovascular Glaucoma
•  Neovascular membrane has grown over the surface of the
chamber, smoothing the iris folds and crypts
•  Myofibroblasts cause contraction and apposition of the
trabecular meshwork – outflow is blocked, inc IOP

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Open Angle Glaucoma
•  Signs and symptoms
–  Initially asymptomatic/painless
–  Incidental finding on comprehensive eye
examination
–  Initially gradual loss of bilateral peripheral vision
–  Loss of central vision – late manifestation
–  Blindness (if left untreated)

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Open Angle Glaucoma
•  Clinical Interventions
–  Beta-blockers
•  Reduces production of aqueous humor by the ciliary
body, which is physiologically activated by cAMP.
•  Timolol
–  Prostaglandin F2, alpha-adrenergic-2 agonists,
Pilocarpine, carbonic anhydrase inhibitors

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Clinical Interventions
•  Laser Trabeculoplasty/Surgical Trabeculectomy
•  Iridotomy
–  This makes a tiny hole in the iris to let fluid flow more
freely
•  Microsurgery
–  implantation of a tube to help drain fluid
–  temporary or permanent vision loss, as well as
bleeding or infection.

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

OUR LADY OF FATIMA UNIVERSITY
COLLEGE OF PHARMACY

Autonomic Nervous System

Disorders:
Myasthenia Gravis
CLINICAL PHARMACY AND
PHARMACOTHERAPEUTICS
PHCP311
 Myasthenia Gravis
•  Myasthenia gravis is an autoimmune disease
that is usually associated with autoantibodies
directed against ACh receptors.
–  It has a prevalence of 150 to 200 per 1 million and
shows a bimodal age distribution. In young adults,
the female-to-male ratio is 2:1, but in older adults
there is a male predominance

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Myasthenia Gravis
•  Anti–ACh receptor antibodies are thought to lead to
the aggregation and degradation of the receptors, as
well as to damage of the postsynaptic membrane
through complement fixation.
–  As a result, postsynaptic membranes show
alterations in morphology and are depleted of
ACh receptors.

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Myasthenia Gravis
•  There is a strong association between pathogenic
anti–ACh receptor autoantibodies and thymic
abnormalities.
–  Approximately 10% of patients with myasthenia gravis
have a thymoma, a tumor of thymic epithelial cells.
–  An additional 30% of patients (and particularly young
patients) have a different thymic abnormality called
thymic hyperplasia.
•  This peculiar condition is marked by the appearance
of B-cell follicles in the thymus.

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Clinical Features
•  Patients with anti–ACh receptor antibodies
typically present with fluctuating weakness
that worsens with exertion and often over the
course of the day.
–  Prominent bulbar findings - diplopia, and ptosis,
dysphagia, dysarthria, and/or weakness, often
with fatiguability.

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Diagnostic Tests
•  Based on clinical history, physical findings,
identification of autoantibodies, and
electrophysiologic studies.
–  Electrophysiologic studies reveal a decrement in
muscle response with repeated stimulation, a
characteristic of this disorder.

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Clinical Interventions
•  Cholinesterase inhibitors (carbamates)
–  Forms covalent bond with AchE, but hydrolyzed and
release
–  Like edrophonium, but longer-acting
–  Neostigmine, Pyridostigmine
•  Plasmapheresis(plasma exchange)
–  removes harmful antibodies from the blood
–  short-term treatment
•  Intravenous immune globulin (IVIG)
–  it affects the creation and function of antibodies

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

 Clinical Interventions
•  Thymus gland removal
–  Removal of the thymus gland, which is part of the
immune system, may be appropriate for many
patients with MG.
–  Once the thymus is removed, patients typically show
less muscle weakness.
•  Non-pharmacological
–  Get plenty of rest to help minimize muscle weakness.
–  Avoid stress and heat exposure, as both can worsen
symptoms

OUR LADY OF FATIMA UNIVERSITY – COLLEGE OF PHARMACY – PHCP311

CLINICAL PHARMACY
AND THERAPEUTICS I
STROKE
STROKE
¨  Stroke involves abrupt onset of focal
neurologic deficit that lasts at least 24 hours
and is presumed to be of vascular origin.
Stroke can be either ischemic or hemorrhagic.
¨  Transient ischemic attacks (TIAs) are focal

ischemic neurologic deficits lasting less than

24 hours and usually less than 30 minutes.
¨  It is the second leading killer worldwide.
¨  It is the leading cause of adult disability.

¨  Approximately 20% of patients in nursing

homes have had a stroke.
¨  Also one of the most expensive diseases
due to expensive posthospitalization care.
¨  Deaths from stroke is still expected to
rise.*
ISCHEMIC STROKE
¨  Ischemic strokes (87% of all strokes) are due either to
local thrombus formation or emboli occluding a
cerebral artery. Cerebral atherosclerosis is a cause in
most cases, but 30% are of unknown etiology.
¨  Emboli arise either from intra- or extracranial arteries.
Twenty percent of ischemic strokes arise from the
heart.
¨  Carotid atherosclerotic plaques may rupture, resulting
in collagen exposure, platelet aggregation, and
thrombus formation. The clot may cause local
occlusion or dislodge and travel distally, eventually
occluding a cerebral vessel.
¨  In cardiogenic embolism, stasis of blood flow
in the atria or ventricles leads to formation of
local clots that can dislodge and travel through
the aorta to the cerebral circulation.
¨  Thrombus formation and embolism result in

arterial occlusion, decreasing cerebral blood

flow and causing ischemia and ultimately
infarction distal to the occlusion.
¨  Sudden loss of blood circulation to an area of
the brain, resulting in a corresponding loss of
neurologic function.
¨  Acute ischemic stroke is caused by thrombotic

or embolic occlusion of a cerebral artery.

¨  Cerebral ischemia à breakdown of BBB within
4-6 hoursà vasogenic edema: proteins and
water flood into the extracellular wall.à
swelling
Clotting due to atherosclerosis

¨  Lipid accumulation with inflammatory cells would

eventually result to plaque formation.
¨  Sheer stress could rupture the plaque and cause
clots.
¨  Clot will remain and occlude the blood vessel
leading to ischemia distal to the occlusion. OR
¨  Clot that formed due to stasis of blood in the
Atrium* will cause clots that could travel (emboli)
Ischemia due to decreased blood flow

¨  Normal cerebral blood flow averages at

50mL/100g per minute.
¨  When local cerebral blood flow decreases
below 20 mL/100 g per minute, ischemia
ensues.
¨  And If below 12 mL/100 g per minute persist,
irreversible damage to the brain or infarction
happens.
HEMORRHAGIC STROKE
¨  Hemorrhagic strokes (13% of strokes) include
subarachnoid hemorrhage (SAH) and
intracerebral hemorrhage. SAH may result
from trauma or rupture of an intracranial
aneurysm or arteriovenous malformation
(AVM).
¨  Intracerebral hemorrhage occurs when a

ruptured blood vessel within the brain causes

a hematoma.
¨  Blood in the brain parenchyma causes
mechanical compression of vulnerable tissue
and subsequent activation of inflammation and
neurotoxins.
¨  Not as well studied as Ischemic stroke
¨  When blood is present in the brain, the

neurotoxicity of the components of blood

and their degradation products could
damage the brain.
¨  Hemorrhage volumes >60 mL are associated

with 71% to 93% mortality at 30 days.

¨  Most early deaths is caused by the abrupt

increase in intracranial pressure

¨  Bleeding occurs directly into the brain
parenchymaà leakage from small
intracerebral arteries due to hypertension
¨  Seizure is more common in hemorrhagic

stroke that in ischemic stroke

¨  Low glasgow coma scaleà poorer prognosis
and mortality
¨  Patients may be unable to provide a reliable
history because of neurologic deficits.
¨  Family members or other witnesses may need

to provide this information.

¨  Symptoms include unilateral weakness,

inability to speak, loss of vision, vertigo, or

falling. Ischemic stroke is not usually painful,
but headache may occur in hemorrhagic
stroke.
¨  Neurologic deficits on physical examination
depend on the brain area involved.
¨  Hemi- or monoparesis and hemisensory
deficits are common. Patients with posterior
circulation involvement may have vertigo and
diplopia.
¨  Anterior circulation strokes commonly result in
aphasia. Patients may experience dysarthria,
visual field defects, and altered levels of
consciousness.
Causes
¨  Hypertension
¤  Hypertensive
small vesselsà results in tiny
aneurismsà ruptureà inter parenchymal
hemorrhage
¨  Cerebral angioedema
¤  Due to the mutation in the amyloidal precursor
proteins
¤  Inherited

¨  Coagulopathy: deficiency in the factors

¨  Depends on the area of affectation
¨  Usually affects the left side

¤  Right hemiparesis:
n  Weakness of the portion or side of the body
¤  Right hemisensory loss
¤  Left gaze preference
n  Tonic deviation of eve towards the side of injury.
¤  Rightvisual field cut
¤  aphasia
Clinical Presentation
Symptoms
¨  One-sided weakness

¨  Inability to speak

¨  Loss of vision

¨  Vertigo / Falling

¨  Not painful if Ischemic

¨  Very painful if Hemorrhagic

Signs
¨  Patients usually have multiple signs of neurologic
dysfunction,
¨  and the specific deficits are determined by the area of
the brain involved.
¨  Monoparesis – one limb is weak but not paralyzed

¨  Patients with vertigo and double vision are likely to

have posterior circulation involvement.
¨  Aphasia is seen commonly in patients with anterior
circulation strokes.
¨  Patients also may suffer from dysarthria, visual field
defects, and altered levels of consciousness.
Diagnosis
¨  Laboratory tests for hypercoagulable states
should be done only when the cause cannot be
determined based on presence of risk factors.
Protein C, protein S, and antithrombin III are best
measured in steady state rather than in the acute
stage.
¨  Antiphospholipid antibodies are of higher yield but
should be reserved for patients younger than 50
years and those who have had multiple venous or
arterial thrombotic events or livedo reticularis.
¨  Computed tomography (CT) and magnetic
resonance imaging (MRI) head scans can
reveal areas of hemorrhage and infarction.
¨  Carotid Doppler (CD), electrocardiogram

(ECG), transthoracic echocardiogram (TTE),

and transcranial Doppler (TCD) studies can
each provide valuable diagnostic information.
Ischemic
¨  Intravenous tissue plasminogen activator
within 3 hours of onset.
¨  Every 15 minutes × 1 hour; every 0.5 h ×
6 h; every 1 hour × 17 hour
¨  Aspirin within 48 hours of onset. Should
not be given 24 hours after tPA – risk of
bleeding.*
¨  Address comorbidities
¤  Hyperthermia : accelerates during neuronal injury
n  Acetaminophen for fever >100.4F
¤  Oxygen saturation <95%
n  Supplemental oxygen
¤  Hyperglycemia:common after acute ischemic
attack even without diabetes
Fibrinolytic therapy
¨  Streptokinase increases the risk for intracranial
hemorrhage and death.
¨  Recombinant Tissue Plasminogen activator
¤  Alteplase
¤  Restores cerebral blood flow and leads to
improvement or resolution of neurologic deficits,
¤  May cause intracranial bleeding, Angioedema and
allergic reactions
¤  Should be given within 3-4.5 window period after the
onset of stroke and only after ruling out hemorrhagic
stroke via CT scan
Antiplatelet
¨  Aspirin 325 mg with in 24-48 hours
¨  For immobilized stroke patients: predisposed

to DVT or deep venous thrombosis:

¤  Providelow dose, unfractionated low molecular
weight heparin.
¨  Hemorrhagic:
¤  Depends on the cause and severity of bleeding.
¤  Basic life support, control of bleeding, seizure, BP
and intracranial pressure are critical.
¤  Anticonvulsants: to prevent seizure recurrence

¤  Osmotic diuretic: to reduce intracranial pressure

in the subarachnoid space.
NO EEFECTIVE TARGETED THERAPY FOR
HEMORRAHIC STROKE.