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Spring 2018 > Pharm Test 3 > Flashcards

Pharm Test 3 Flashcards

1
Q

2 things that cause heart failure

A

Can’t fill heart with enough blood (diastolic)

Can’t pump enough blood (systolic)

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2
Q

Pumping less than _ constitutes heart failure

A

40 to 50%

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3
Q

Causes of heart failure (12)

A 
MI
Coronary artery disease
Valve disease
Idiopathic cardiomyopathy
Viral/bacterial cardiomyopathy
Myocarditis
Pericarditis
Arrhythmias
Chronic hypertension
Thyroid disease
Pregnancy
Septic shock
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4
Q

Class I-IV heart failure

A

1-mild-normal
2-mild-slight limitation of physical activity
3-moderate-limitation of activity, less than normal activity causes fatigue
4-severe-can’t do any physical activity w/o discomfort

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5
Q

Excitation-contraction coupling:

A

Action potential in skeletal or cardiac muscle triggers muscle contraction

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6
Q

Cardiac muscle contraction is the result of _

Causing _

Which _

A 
Ca influx from depolarization
-Causing
Release of more Ca from SR
-Which
Binds to troponin causing interaction b/t actin and tropomyosin
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7
Q

T/F Skeletal and Cardiac muscle get Calcium the same way

A

False

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8
Q

Depolarization of _ leads to opening of voltage gated Ca channels

A

Cardiac myocyte

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9
Q

Receptors on SR that, when activated, lead to more Ca release

A

Ryanodine

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10
Q

Ca binds to _ which alters the interaction b/t _ and _, exposing _ binding sites on _

A

binds to TROPONIN which alters interaction b/t TROPOMYOSIN and ACTIN exposing MYOSIN binding sites on ACTIN

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11
Q

6 factors that contribute to how well the heart pumps blood

A
  1. Sensitivity of contractile proteins to Ca
  2. Amount of Ca that is released
  3. Amount of Ca stored in SR
  4. Amount of Ca that enters cell at depolarization
  5. Activity of Na/Ca exchanger
  6. Intracellular Na conc. And activity of Na/K ATPase
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12
Q

Inotropic vs. chronotropic drugs

A

Ino-alter force or energy of muscular contractions

Chrono-change heart rate by affecting nerves controlling heart, or by changing rhythm of SA node

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13
Q

3 positive inotropic drugs to treat heart failure

A
  • cardiac glycosides
  • B-adrenergic receptor
  • Bipyridines
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14
Q

Cardiac glycosides used in US

A

Digoxin

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15
Q

Digitalis:

A

Name for any cardiac glycoside

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16
Q

How does digoxin work

A

Blocks Na/K ATPase

-internal Na increases, slowing Na/Ca exchanger, slowing removal of Ca

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17
Q

Digoxin, and therefore altering Na/K ATPase messes with

A

Electrical activity of the heart

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18
Q

Most popular B-1 adrenergic receptor agonists

A

Dobutamine

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19
Q

T/F B1-adrenergic receptor agonists are the first line of defense

A

FALSE

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20
Q

4 drugs that treat both systolic and diastolic heart failure

1 for systolic only

A

ACE inhibitor
Diuretic
Spironolactone
B-blocker

Digitalis

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21
Q

Bipyridines act how

A

They are phosphodiesterase-3 inhibitors

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22
Q

Main drug w/o positive inotropic effects used to treat heart failure

A

B-adrenergic receptor ANTAGONISTS (beta blockers)

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23
Q

Medications for CHF can cause

A

Dry mouth and gingivitis

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24
Q

_% of patients with heart disease also have periodontitis

A

91

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25
Q

3 types of angina

A
  1. Classical/stable-due to fixed and stable plaque
  2. Variant-spasm of coronary artery
  3. Unstable-due to unstable plaque
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26
Q

Stable angina vs. acute coronary syndrome

A

Stable:
Symptoms related to effort
Predictable

Acute coronary:
Unpredictable
Symptoms at rest

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27
Q

5 drugs used to treat angina

A 
Nitrates/nitrites
B-adrenergic receptor blockers
Ca channel blockers
Aspirin, anticoagulant drugs
Ranolazine
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28
Q

Nitrates and nitrates are _ that spontaneously produce _

A

Prodrugs

Nitric oxide

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29
Q

_ compounds are ineffective drugs for angina. Example is _

A

Inorganic compounds

Na nitrite, used for cyanide poisoning

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30
Q

How is nitroglycerin applied, and what does it treat

A

Apply under tongue

Acute episodes of angina

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31
Q

Adverse effects of nitrates/nitrites

A 
Headache
Hypotension
Facial flushing
Tachycardia
Dangerous if used with viagra
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32
Q

Beta adrenergic receptor blockers (beta blockers)
Do what at the SA node?
Do what at the ventricular myocardium?

A

SA: decrease heart rate

VM: decrease contractility

BOTH: decrease O2 demand

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33
Q

Ca channel blockers do what

A

Same as beta blockers in heart

AND
Increase vasodilation
Increase O2 supply

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34
Q

To treat angina:

Vasodilators:

Cardiac Depressants:

Both:

A

VD: nitrates
CD: beta blockers
Both: calcium blockers

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35
Q

4 steps in kidney function

A

Filtration
Resorption
Secretion
Excretion

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36
Q

70% of filtered Na is resorbed in what part of the renal tubule?

Why

A

PCT

Carbonic anhydride inhibitors

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37
Q

What does carbonic anhydrase do specifically?

SO, CA inhibitors end up doing what

A

Facilitates Na and HCO3 reabsorption (and therefore H2O retention

Inhibitors enhance fluid loss (water follows Na)

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38
Q

Where do you find osmotic diuretics

What is an OD

A

PCT, PST

Diuretic that inhibits reabsorption of water and Na

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39
Q

Mannitol is an osmotic diuretic, how does it work?

A

It isn’t reabsorbed well, it keeps water in urine

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40
Q

Loop diuretics are found where

A

Thick ascending limb of loop of henle

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41
Q

What do loop diuretics treat and how

A

Treat hypertension

By

Inhibiting Na, K, 2Cl symporter
(Increases the excretion of these)

Water follows

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42
Q

Loop diuretics are derivatives of what? Why is this important

A

Sulfonamide derivatives

Many people are allergic to sulfonamides

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43
Q

Thiazide diuretics are found where

A

Distal convoluted tubule

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44
Q

What do thiazide diuretics do

A

Block Na/Cl symporter
Increase Na/Cl excretion
Water follows

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45
Q

Why are K sparing diuretics necessary

A

Loop and thiazide diuretics increase Na delivery to distal segment of Distal tubule which increases potassium loss.

This happens because the aldosterone sensitive Na pump increases Na conc. in exchange for K and H+

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46
Q

K sparing diuretics work where

A

Cortical collecting tubule

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47
Q

MAP=

A

CO x TPR

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48
Q

How does the baroreflex regulation system work?

Baroreceptors send BP info to _

Symp. Nerves adjust _ to regulate vasoconstriction, heart beat and CO

A

Baroreceptors send BP info to medulla

Catecholamines

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49
Q

What cells in kidney have baroreceptors

A

JG cells

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50
Q

In kidneys, BP decrease causes what

A

Na decrease in infiltrate
Sympathetic stimulation
And
Renin release from JG apparatus into plasma

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51
Q

Renin does what

A

Converts angiotensinogen to angiotensin 1

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52
Q

Where is angiotensinogen made and what does it do

A

Made by liver

Becomes angiotensin 1

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53
Q

What is ACE and what does it do

A

Angiotensin converting enzyme

Converts angiotensin I to angiotensin II

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54
Q

What effects do:
Angiotensinogen
Angiotensin I
Angiotensin II

Have on Na resorption

A

Only angiotensin II mediates vasoconstriction, Na resorption, and water retention

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55
Q

Why use an ACE inhibitor? What do they do?

A

Prevent hypertension

Prevents angiotensin I from becoming angiotensin II

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56
Q

Angiotensin II promotes _ release from _

A

Aldosterone release from adrenal cortex

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57
Q

4 drugs to treat hypertension

A

Diuretics
Sympathoplegic agents
Direct vasodilators
Angiotensin II blockers

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58
Q

Person with mild to moderate hypertension is recommended _

A

Thiazide

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59
Q

Sympathoplegic agents do what

A

Reduce release of epinephrine from sympathetic nerve endings

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60
Q

4 types of direct vasodilators

A

Nitric oxide pro-drugs

Drugs that reduce Ca influx into vascular smooth muscle

Drugs that cause Hyperpolarization of vascular smooth muscle

Drugs that activate dopamine receptors

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61
Q

Suffix -pril usually denotes what

A

Prodrug, especially ACE inhibitor

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62
Q

Suffix -sartan indicates a drug that does what

A

Blocks angiotensin II production or activity

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63
Q

4 types of arrhythmias

A

Extra beats
Supraventricular tachycardia
Ventricular arrhythmia
Bradyarrhythmia

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64
Q

4 places from which arrhythmias can originate

A

Atria
Ventricle
Junction
AV node (av block)

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65
Q

AV blocks:

1˚, 2˚, 3˚

A

Conduction b/t atria and ventricles is blocked or slowed causing arrhythmia

1˚- PR interval beyond 0.2 seconds
2˚-disturbance, delay or interruption of atrial impulse conduction through AV node to ventricles
3˚- complete heart block. Impulse from SA node doesn’t propagate to ventricles

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66
Q

4 causes of arrhythmias

A

Cardiac ischemia
Excessive discharge or sensitivity to autonomic transmitters
Exposure to toxic substances
Unknown? Other?

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67
Q

4 classes of antiarrhythmic drugs

A

I-block Na channels
II-Block B-adrenoceptor antagonists
III-prolong action potential and refractory period (K channel blockers)
IV-Block Ca channels

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68
Q

Why does blocking B-adrenergic antagonists work to treat arrhythmias?

A

Excess stimulation of beta receptors can lead to arrrhythmias

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69
Q

How does blocking K channels treat arrhythmias

A

It delays repolarization and prolongs action potential and refractory period

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70
Q

High levels of free fatty acids contribute to what

A 
Insulin resistance
Heart disease
Atherosclerosis
Metabolic syndrome
Obesity
Cancer
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71
Q

Dyslipidemia:

A

Disorder of lipoprotein metabolism

Includes overproduction and deficiency

72
Q

5 types of drugs used to treat dyslipidemia

A
  1. Fibric Acid and derivatives
  2. Nicotinic Acid
  3. Bile Acid sequestrants
  4. Inhibitors of HMG CoA reductase (statins)
  5. Cholesterol Absorption inhibitors
73
Q

What does fibric acid do

How

A

Reduce levels of triglycerides

Agonists of PPARalpha
-combined with RXR-alpha regulate gene expression
—Those genes regulate cell differentiation & development and carb and lipoid and protein metabolism

74
Q

Side effects of fibric acid derivatives

A

Abdominal pain, diarrhea, nausea
Blurred vision
Gallstones
Long prothrombin time

75
Q

Nicotinic acid, AKA _ can treat dyslipidemia

A

Niacin

76
Q

How does nicotinic acid work

A

Agonist for GPR 109A/B receptor

Inhibits diacylglycerol acyltransferase

77
Q

What does DGAT do

A

Takes 1,2 DAG to triacylglycerol

78
Q

Receptor that niacin agonizes

Activation inhibits what

A

109A/B

Activation inhibits lipolysis and atherogenic activity

79
Q

Two major benefits of niacin therapy

A

More HDL

Less triglyceride

80
Q

Side effects of nicotinic acid

A

Flushing
Itching (pruritis)
GI distress

81
Q

How do bile acid sequestrants work? Why sequester bile acid?

A

Drugs keep bile acids from getting absorbed in intestines, are pooped out

Why?
-Bile acids are made when liver converts cholesterol to bile acid, more pooped out, more will be metabolized

82
Q

Why block HMG CoA reductase?

A

In pathway to synthesize cholesterol

83
Q

Who should take statins

A

Men
Over 65
No Hx of heart disease
Don’t have current problems
1+ risk factors (high cholesterol, diabetes, etc)
10% risk of heart attack in next 10 years

84
Q

Cholesterol absorption inhibitors overall do what

A

Inhibit LDL formation

85
Q

The transport protein that moves cholesterol from lumen into enterocyte:

Blocked by:

A

NPC1L1

Blocked by ezetimibe

86
Q

Side effects of cholesterol absorption inhibitors

A

GI pain/diarrhea

87
Q

Normal fasting blood glucose

A

70-100 mg/dL

88
Q

α cells secrete:
β cells secrete:
δ cells secrete:

A

α: glucagon
β: insulin
δ: somatostatin

89
Q

How does glucagon work to raise blood sugar levels (5 steps)

A 
GPCR
Elevates cAMP levels
Activate PKA
Kinase cascade
Liberation of glucose from glycogen
90
Q

Receptor that insulin binds to

3 major biochemical effects that can result

A

Tyrosine Kinase Receptor

  1. Decrease in blood glucose levels
  2. Promotion of storage of fat
  3. Enhancement of protein anabolism
91
Q

DM vs DI

A

DM: metabolic disorder, high blood sugar levels over prolonged period

DI: large amounts of dilute urine and increased thirst

92
Q

DM type 1:
What’s going on w/insulin
Blood sugar?
Cause:

A
  • Not enough insulin produced
  • High blood sugar
  • Immune system destroys β cells in pancreas
93
Q

What is secondary diabetes

A

β cells destroyed not by immune cells, but something else like disease or injury

94
Q

DM type 2:
Sugar?
Insulin?
Causes?

A

High blood sugar
Insulin resistance, lack of insulin
Obesity and bad lifestyle, genes too

95
Q

Gestational diabetes:
3 risks?
Risk to baby?

A

Pre-eclampsia, depression, c-section

Baby can be overweight, low blood sugar, jaundice, getting type 2 diabetes

96
Q

Peak age for diagnosis of type 1 diabetes

A

14

97
Q

3 targets of insulin

A

Liver, adipose, skeletal muscle

98
Q

3 acute complications of diabetes

A
  1. Diabetic ketoacidosis
  2. Hypersomolar hyperglycemic state
  3. Hypoglycemia
99
Q

What is diabetic ketoacidosis

A

Liver converts pyruvate to glucose
Liver gets pyruvate from skeletal muscle
Results in excess keto acid

ALSO

Liver oxidizes fatty acid to Acetyl CoA
Liver converts ACoA to ketone bodies

100
Q

Hyperosmolar hyperglycemic state:
Features

When?

A

Hyperosmolar plasma
Dehydration
Hyperglycemia

Type 2 DM, with physiologic stress

101
Q

How are vascular complications from diabetes induced?

A

Through diabetes induced endothelial cell dysfunction

ROS

  • enhanced in hyperglycemia
  • consequence of oxidative rxns
102
Q

4 tests to diagnose diabetes

A
  1. A1C
  2. Fasting glucose
  3. Casual Blood glucose
  4. Oral glucose tolerance test
103
Q

Normal fasting and post meal blood sugar levels

A

F: 70-100mg/dL
PM: 70-140mg/dL

104
Q

A1C test measures what

Why is it good

A

Glycation of hemoglobin

Hemoglobin lasts 115 days, so its value is an average over a longer time

105
Q

How to administer oral glucose tolerance test?

Normal baseline
1 hr
2 hr

A

Draw blood
Give 75 g of glucose
Draw blood after 1 and 2 hr

Normal:<110mg/dL

1hr: <180 mg/dL
2hr: <140mg/dL

106
Q

Secretagogues

A

Molecules/drugs that affect insulin secretion by affecting glucose sensors

107
Q

Incretins:

A

Drugs that work on GLP-1 receptors on β cells and stimulate insulin release

108
Q

First line of treatment for type 2 diabetes

A

Metformin (Biguanide)

109
Q

What does metformin do

A
  • Doesn’t stimulate insulin secretion
  • Increases glucose uptake and use in sk muscle
  • Reduces hepatic glucose production
110
Q

T/F metformin enhances action of glucagon

A

FALSE - it opposes glucagon

111
Q

How does metformin work? (Popular theory)

A

Activation of AMP-dependent protein kinase

112
Q

What do thiazolidinediones do

A

Decrease insulin resistance

113
Q

How do α-glucosidase inhibitors work

A

Inhibit the digestion of glucose

114
Q

3 steps of clot formation

A

Vessel constriction

Platelet adhesion, activation, aggregation

Cross-linking of fibrin thru coagulation cascade

115
Q

2 molecules produced by endothelial cells upon injury

What do they do

A

Prostaglandin F 2α
Τhromboxane A2

Vasoconstriction to limit hemorrhage

116
Q

In platelet adhesion, what do platelets adhere to

A

Matrix protein’s collagen
Fibronectin
vWF

117
Q

What is secreted by activated platelets (4)

A

PGF2α
Thromboxane A2
ADP
Serotonin

118
Q

Platelets aggregate as a result of _, forming the platelet plug

A

Fibrinogen cross-linking

119
Q

_ is cleaved by _ to form fibrin

A

Fibrinogen is cleaved by thrombin to form fibrin

120
Q

Extrinsic pathway (6 steps)

A 
TF
VII->VIIa
IX->IXa
X->Xa
                             (Xa+Va)
Prothrombin(II) —————>thrombin(IIa)
                        (Thrombin)
Fibrinogen(I) ——————>fibrin(Ia)
121
Q

In addition to activating I->Ia, thrombin also activates what 3 other factors

A

V
VIII
XI

122
Q

What does factor XII do

A

Starts intrinsic pathway (XII, XI, IX, X)

Cross links fibrin mesh

123
Q

Antithrombin is a _
It is produced by _
It’s activity is increased by _, which enhances binding of _ to _ and _

A

Serine protease inhibitor

the liver

Heparin which enhances binding of antithrombin to factor II (thrombin) and factor X

124
Q

Protein C inactivates what two proteins

It is classified as a _

How is it activated

A

Factor Va and VIIIa

Serine protease

Activated by binding to thrombin

125
Q

Tissue factor pathway inhibitor is a _

It can reversible inhibit _ and _ together

A

Single chain polypeptide

Xa and VIIa-TF complex

126
Q

DIC:

A

Disseminated intravascular coagulation - widespread activation of clotting cascade, clots form in small vessels throughout body

127
Q

5 fibrinolytics

A 
Streptokinase
Urokinase
Reteplase
Alteplase
Tenecteplase
128
Q

Types of anti-coagulant drugs

A
  1. Indirect thrombin inhibitors

2. Direct thrombin inhibitors

129
Q

Heparin is a _

It acts on _

A

Indirect thrombin inhibitor

AT

130
Q

Hirudin is a _

It is found in _

A

Direct thrombin inhibitor

Leeches

131
Q

_ is an oral direct thrombin inhibitor. One of these is _

A

Coumarin

Warfarin

132
Q

For thrombin to become catalytically competent, it needs to undergo a _ rxn

This requires the _ of _

Coumarins block _

Without this, the body runs out of reduced vitamin K and thrombin won’t become active.

A

Carboxylation

Oxidation of vitamin K

The conversion of oxidized vit. K back to reduced form

133
Q

What are some drugs that interact with warfarin

A 
Antibiotics
Antifungals
Antidepressants
Antiplatelet agents
Anti-inflammatory agents

Amiodarone
Acetaminophen
Alternative remedies

134
Q

Antidote for warfarin overdose

A

Vit. K

135
Q

3 things that block platelet aggregation

1 thing that promotes platelet aggregation

A

Aspirin
Clopidogrel
Epifibatide

Thromboxane A2

136
Q

3 essential nutrients for Hematopoiesis

A

iron
Vit B12
Folic acid

137
Q

Heme is made where

A

Mainly in liver and bone marrow. Half in mitochondria, half in cytosol

138
Q

Iron excretion:

A

Mostly through blood. Why women lose a lot in menses.

Feces has unabsorbed, lost skin cells another avenue.

139
Q

Iron is transported into plasma bound to _

It’s stored in _ found in _

A

Transferrin

Ferritin, liver spleen bone marrow

140
Q

Anemias from lack of B12 usually reflect a _

A

Problem with absorption

141
Q

Folic acid deficiency can cause _ and _

B12 deficiency can cause _

A

Megaloblastic anemia
Glossitis

Neurologic disease

142
Q

Treatment of sickle cell

A

Marrow donor

143
Q

Erythropoietin (EPO) is used to treat anemia from what

A

Chronic kidney disease
Inflammatory bowel disease
Myelodysplasia from tx of cancer

144
Q

G-CSF, GM-CSF, IL-11 are what

Used to do what

A

Hematopoietic growth factors

Stimulates bone marrow to make granulocytes and stem cells and release them

145
Q

Ant. Pit hormones that are used as drugs

A

FSH
LH
GH

146
Q

A receptor with associated with _ mediates the effects of GH

A

JAK kinase

147
Q

What kind of molecule is GH

How big is it

A

191 aa polypeptide

148
Q

FSH and LH:
Regular actions
Follicular stage actions
Luteal stage actions

A

Regular:

  • (FSH) Ovarian follicle development
  • (Both) Ovarian steroidogenesis

Follicular:

  • (LH) Androgen production
  • (FSH) conversion of androgens to estrogens

Luteal:
-(LH) estrogen and progesterone production

149
Q

In men:
FSH action
LH action

A

FSH: spermatogenesis
LH: testosterone production

150
Q

Vasopressin acts on two different receptors. Which has which effect?

A

V1: vasoconstriction, increased arterial pressure
V2: increased blood volume

151
Q

Clinical vasopressin treats 3 things

A

Diabetes insipidous
Bleeding problems
Nocturnal enuresis

152
Q

2 causes of diabetes insipid is

A

Central - can’t make or secrete ADH

Nephrogenic - kidney can’t respond to ADH

153
Q

Why give/suppress oxytocin

A

Give: induce labor

Suppress: halt premature labor

154
Q

ADH or vasopressin does what

A

Pee less, retain water, higher blood pressure

155
Q

T4 is dominant in _

T3 is more _

A

Plasma

Active

156
Q

3 ways to treat hyperthyroidism

A

Thioamides-block hormone synthesis

Anion inhibitors - block I transport into thyroid

Iodide

157
Q

Body is low on Ca. What happens

A

PTH released
Bone resorption increased
Ca elimination in kidneys decreased
Ca absorption increased in gut

158
Q

Calcium and _ block PTH release

A

Vitamin D (thru gene expression)

159
Q

PTH acts on _ receptor in bone and kidney. Activation causes expression of _. This leads to activation of osteoclasts and bone resorption

A

PTHR1

RANK ligand

160
Q

Effects of PTH on kidney

A

Ca resorption
PO4 decrease resorption
Vitamin D production

161
Q

The active form of vitamin D is _. _ enhances its production. This enhances _

A

Calcitrol
PTH
Absorption of Ca from gut

162
Q

Vitamin D does more than influence Ca. Other things it does

A 
Brain development/function
Reduce inflammation
Heart function
Blood pressure
Reduce colon cancer
Muscle strength
163
Q

Calcitonin is released by _ cells of the _ in response to high serum Ca

A

Parafollicular cells of thyroid

164
Q

Dental abnormalities from hyperparathyroidism

A 
Pulp chamber obliteration by pulp stone
Alteration in eruption
Loosening and drifting of teeth
Perio ligament widening
Tori
165
Q

Dental abnormalities from hypoparathyroidism

A 
Enamel hypoplasia
Delayed eruption
Hypodontia
Poorly calcified dentin
Widened pulp chambers
Ankylosis
Caries

(Not enough Ca for teeth)

166
Q

Osteoporosis can be treated with _.

They do what

A

Bisphosphonates

Prevent loss of bone mass

167
Q

Most testosterone (95%) comes from _

A

Leydig cells of testes

168
Q

3 natural estrogens

Major product of ovary is _

A

Estrone (E1)
Estradiol (E2)
Estriol (E3)

Major is E2

169
Q

Clinical uses of estrogen

A

Primary hypogonadism
Postmenopausal hormone therapy
Suppress ovulation/ovarian function

170
Q

What is tamoxifen?

When is it used

A

Inhibits estrogen receptor positive cell proliferation

Used when cells are estrogen receptor positive to stop cells dividing

171
Q

How do estrogen nuclear receptors work

A

Agonist exposes AF-2 region of receptor
Co-activators can only bind if it is exposed
Agonists bind well but don’t cause conformation change

172
Q

What is a SERM

A

Selective estrogen receptor modulator

Can be an agonist or antagonist depending on co-activator availability

173
Q

Progestins are made in what 3 places

They are precursors to what 3 things

A

Corpus luteum
Placenta
Adrenal cortex

Androgens
Estrogens
Adrenocortical hormones

174
Q

Two types of oral contraceptives

How do they work

A

Estrogen + progesterone
-block LH and FSH release from pit

Progesterone only

  • thickening of cervical mucus (blocks sperm)
  • block release of eggs from ovary
175
Q

2 emergency oral contraceptives

A
  1. Higher dose of oral contraceptives

2. RU486 (progesterone partial agonist)

Spring 2018 (18 decks)

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