Midterm 2 Review Flashcards
Hypertension
- PCNS vs SNS NT
- PCNS vs SNS Receptor type
- 4 ways of regulation BP
- Main HT diagnosis
- Relationship between BP and age
- Why is HT treated late?
- Coarctation of aorta
- Pheochromocytoma
- Cushing’s disease
- 4 major drug groups for HT
- ACh vs NE
- Muscarinic cholinergic vs alpha (vessels)/beta (heart)
- a) Resistance via arterioles (a1 cause vasoconstriction)
b) Capacitance via venules
c) Pump output (HR, contraction)
d) Renin –> Angiotensin –> Aldosterone - Repeated, elevated BP
- Older = higher BP
- Asymptomatic until overt organ damage imminent or has happened
- Constriction of aorta
- Tumors in adrenal medulla produce excess adrenaline
- Tumors in pituitary gland makes too much adrenocorticotropic hormone
- Diuretics, Sympathoplegics, Vasodilators, Angiotensin antagonists
Hypertension
- 2 types of diuretics and a name for each
- Mechanism of both drugs and effect
- Toxicity in both
- 4 types of sympathoplegics
- Thiazides (hydrochlorothiazide) and loop diuretics (furosemide)
- Thiazide: block Na+/Cl- symporter. Increases Ca2+ reabsorption
Furosemide: block Na+/K+/2 Cl- symporter. Increases Ca2+ excretion - Hypokalemia
- a) Centrally acting agents
b) Ganglion blockers
c) Postganglionic sympathetic neuron blockers
d) Adrenoreceptor blockers
Hypertension
- Name of drug for centrally acting agent
- Mechanism
- Toxicity
- Name for ganglion blockers
- Mechanism
- Toxicity
- Name for postganglionic sympathetic neuron blocker
- Mechanism
- 2 names for adrenoreceptor blockers and mechanism
- 3 types of vasodilators
- Clonidine
- a2-selective agonist
- Sudden cessation causes severe HT
- Trimethaphan
- Blocks nAChR in autonomic ganglia
- Intolerance
- Reserpine
- Blocks uptake
- Prazonin (a1 blocker) and propanolol (beta1 blocker)
- a) Nitrovasodilators
b) K+ channel agonists
c) Ca2+ channel blockers
Hypertension
- Name for nitrovasodilators
- Pharmacology
- Name for K+ channel agonists
- Pharmacology
- 3 names for Ca2+ channel blockers
- Why target L-type Ca2+ channels?
- Which of them is/are vasoselective?
- Which of them is/are cardiac/vasuclar-acting?
- 2 classes of angiotensin antagonists
- Nitroprusside
- NO activates guanylate cyclase, which relaxes vascular smooth muscle by (-) modulating V-gated Ca2+ channels
- Diazoxide
- Opening K-channels for longer = hyperpolarization AND causes elevation of cGMP
- Nifedipine, Verapamil, Diltiazem
- They stay open the longest, so they are a good therapeutic target
- Nifepidine
- Verapamil and Diltiazem
- ACE inhibitors and Angiotensin receptor (of vessels) inhibitors
Hypertension
- Name for ACE inhibitor
- Pharmacology
- Name for angiotensin receptor inhibitor (AT1-type)
- Pharmacology
- 2 things to take into account when performing polypharmacy
- Captopril
- Inhibits conversion of AT1 to AT2 and inhibits breakdown of bradykinin
- Losartan
- Competitive AT1 R blocker
- Maximize efficacy and minimize toxicity
Myocardial Ischemia
- 3 things that determine O2 demand
- 2 things that determine O2 supply
- Where does the pain come from in angina pectoris
- Stable angina
- Unstable angina
- Silent/effort ischemia
- Variant angina
- Myocardial infarction
- Cause of coronary artery spasm
- 3 groups of symptomatic drugs
- Contractile state, HR, wall tension
- AV oxygen difference and regional myocardial distribution (blood flow)
- Accumulation of metabolites in muscle tissues
- Atherosclerotic block of coronary artery
- Rupture of atherosclerotic plaque
- Exercise
- Diffuse coronary spasm
- Heart attack, tissue death
- Unknown
- Nitrates, Ca2+ channel blockers, beta-blockers
Myocardial Ischemia
- Name of nitrate
- Effects (3)
- Effects of Verapamil, Nifedipine, and Diltiazem (2)
- Effects of b-blockers (2)
- Side effect of all symptomatic drugs
- 4 approaches to lower lipid
- Nitroglycerin
- Lower venous return, cardiac size, and diastolic myocardial O2 consumption
- Peripheral vasodilation, reduction of cardiac work
- Reduce BP and cardiac work
- Orthostatic hypotension when sitting or lying down
- a) Inhibit cholesterol synthesis
b) prevent cholesterol reabsorption
c) reduce VLDL secretion
d) increase synthesis of lipoprotein lipase
Myocardial Ischemia
- Name for inhibiting cholesterol synthesis
- Mechanism
- Name for prevention of cholesterol reabsorption
- Mechanism
- Name for reduction of VLDL secretion
- Mechanism
- Name for increase of synthesis of lipoprotein lipase
- Mechanism
- 3 classes of drugs affecting coagulation, fibrinolysis, and platelet aggregation
- Statins (lovastatin)
- Inhibit HMG-Co-A reductase to block the de novo synthesis of cholesterol
- Resins (cholestyramine)
- Non-absorbable macromolecules that bind cholesterol
- Niacin (nicotinic acid, vitamin B3)
- Not well understood
- Fibrates (gemfibrozil)
- Activate peroxisome proliferation-activated receptor-a for lipoprotein lipase synthesis
- a) Anticoagulants
b) Fibrinolysis Drugs
c) Anti-platelets
Myocardial Ischemia
- 2 anticoagulants name
- Mechanism of each
- LMW vs HMW heparin
- Toxicity in warfarin
- 2 fibrinolytic drugs
- Mechanism of each
- 3 names of anti-platelets
- Mechanism of each
- Warfarin and Heparin
- Warfarin: blocks reactivation of vitamin K epoxide (cofactor involved in coagulation) and factors to cofactors II, VII, IX, and X
Heparin: binds factor Xa and antithrombin III - Pure, expensive vs less reliable, cheaper
- Teratogenic
- Streptokinase and tissue plasminogen activators
- Streptokinase: conversion of plasminogen to plasmin
tPA: activation of plasminogen bound to fibrin - Aspirin, Ibuprofen, Ticlopidine
- Asprin: Irreversible. Inhibits platelet cyclooxygenase, inhibiting thomboxane A2 synthesis
Ibuprofen: same as asprin
Ticlopidine: alternative to aspirin when allergic. Inhibit platelet response to secreted ADP at adenosine receptors
Heart Failure
- Systolic HF
- Diastolic HF
- What does Frank-Starling’s Law postulate?
- Class I, II, III, IV HF
- Short-term effects of HF
- Long-term effects of HF
- 4 factors that determine CO
- 7 groups to treat HF
- Can’t contract ventricles: not enough blood pumped
- Stiff heart muscles: not enough ventricle filling
- The heart matches stroke volume to the dynamic changes occurring in preload and thereby regulates ventricular contraction and ejection
- I: Symptoms only during exercise
II: Slight limitation on ordinary activities
III: No symptoms at rest, but easily fatigued
IV: Symptoms even at rest - Haemodynamic changes: low CO, excessive sympathetic discharge, salt/water retention
- Neuroendocrine activation: remodeling, cardiac hypertrophy, cardiac apoptosis
- Preload (arterial pressure), afterload (vascular resistance), contractility, heart rate
- a) Positive inotropic drugs
b) diuretics, angiotensin inhibitors
c) b-blocker
d) b-agonists
e) phosphodiesterase inhibitors
f) vasodilators
Heart Failure
- Name for positive inotropic drugs
- Mechanism and effect
- Name for diuretic
- 2 names for AT antagonists
- Name for b-blocker
- Mechanism
- Name for b-agonist
- Mechanism
- Name for phosphodiesterase inhibitor
- Mechanism
- Name for vasodilator
- Effects
- Cardiac glycosides (Digoxin)
- Block Na/K-ATPase: less Ca2+ leaves, thereby increasing contractility (parasympathetic effects)
- Furosemide
- Captopril and Losartan
- Metoprolol
- Unknown, but may be involved in reduced renin secretion
- Dobutamide
- B1-selective: increased contractility and reduced afterload, so increased CO
- Theophylline
- Increases cAMP in cardiac and vascular tissue = contraction
- Nitroglycerin
- Decrease both afterload and preload, leading to reduced O2 requirements
Menopause
- FSH, LH, Estrone, and Estradiol levels at menopause
- Why does it happen?
- Source of estrogen
- 3 Early symptoms
- 3 Intermediate symptoms
- 2 Late symptoms
- How do ERa and ERb differ?
- ERa locations
- ERb locations
- How do PR a and b isoforms differ
- 2 types of HRT treatment
- FSH and LH: High
Estrone and estradiol: low - Loss of FSH and LH negative feedback systems
- Adrenal and adipose tissue
- Hot flashes, insomnia, moodiness
- Vaginal atresia, bladder dysfunction, skin atrophy
- Osteoporosis, CV disease
- DNA sequence
- Reproductive tract and breasts
- Endothelial cells, bone, prostate
- Alternative splicing
- EPT and ET
Menopause
- EPT’s big advantage over ET
- When to use systemic estrogen?
- Name 1 case where localized E is used?
- Why must HRT be used when ≤ 60 y.o. or within 10 years of menopause onset?
- 2 non-pharmacologic interventions against osteoporosis
- 2 main Pharmacologic interventions
- EPT = lower risk of endometrial cancer associated with E alone
- When experiencing early symptoms
- Vaginal dryness
- Higher risk of CVD when taking HRT 20 years after menopause
- Calcium and Vitamin D supplementation
- Selective Estrogen Receptor Modulators (SERMs) and bisphosphonates
Menopause
- Bisphophonates effect
- Warning against it
- Name of drug that’s 3rd gen.
- Mechanism
- Therefore, where does it only act like estrogen?
- What does Duavee contain?
- Inhibits osteoclast activity
- Possible increased risk of rare type of bone fracture when taking bisphosphonates
- Bazedoxifene
- ERa antagonist and ERb agonist
- Bone and lipids
- Conjugated estrogen and bazedoxifene
Immunosuppression
- 3 therapeutic targets from least to most selective
- 3 types of drugs for immunosuppression
- Cell proliferation, T cell function, Antibody approaches
- a) Glucocorticoid receptor agonists
b) Cytotoxic drugs
c) Antibodies
