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ESUN MS2Unit5 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

CRH stimulates ___ release that leads to eventually release of ___?

A

ACTH/cortisol

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2
Q

Cortisol has negative feedback mechanism to lower ___ and ___ production?

A

CRH and ACTH

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3
Q

What are the 2 function of cortisol?

A

Carb metabolism (stress response)/immune function

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4
Q

Cortisol increase serum ___ level to maintain adequate ___ supply to the brain

A

Glucose/glucose

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5
Q

Cortisol increase or decrease BP?

A

Increase by upregulate alpha-1 receptors

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6
Q

Cortisol has pro or anti-inflammatory effects?

A

Anti-inflammatory

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7
Q

Naturally occurring mineralocorticoids are ___ and ___

A

Aldosterone and DOC

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8
Q

___ has weak mineralocorticoids effect?

A

Cortisol

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9
Q

Glucocorticoid is ___?

A

Cortisol

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10
Q

Cortisol has high/low/similar binding affinity to aldosterone receptor than aldosterone?

A

Similar

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11
Q

What prevents cortisol from binding AR?

A

11beta-HSD2 converts cortisol to cortisone (don’t bind to AR)

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12
Q

When do we use supraphysiological dosage of glucocorticoid?

A

For general anti-inflammatory usage

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13
Q

Pituitary adenoma is also called?

A

Cushing’s disease

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14
Q

Wide purple looking abdominal striae appears in what?

A

Cushing’s syndrome

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15
Q

2 of these positive tests are needed to diagnose Cushing’s syndrome?

A

24-hr urine free cortisol excretion/low dose overnight dexamethasone suppression test/midnight salivary cortisol level

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16
Q

How does dexamethasone suppression test work?

A

Give dexa at night—->act as cortisol—>suppress the release of ACTH and CRH—>decrease cortisol level—>check cortisol level in the morning (normally should be low)

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17
Q

Why dont we use ketoconazole for Cushing’s anymore?

A

Hepatotoxicity

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18
Q

What function does Metyrapone tested for? and how?

A

AP: if AP is normal—>metyrapone blocks cortisol production—>ACTH and 11-deoxycortisol increase (precursor)

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19
Q

Which drug creates glucocorticoid resistance?

A

Mifepristone

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20
Q

Which drug is used to treat cortisol induced psychosis?

A

Mifepristone

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21
Q

What is the side effect of Mifepristone?

A

Adrenal insufficiency

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22
Q

How does Mifepristone causes hypokalemia?

A

High cortisol level overwhelm 11beta-HSD2—>cortisol binds to AR—>hypokalemia

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23
Q

Which drug is for Cushing’s disease?

A

Pasireotide

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24
Q

What are primary and secondary adrenal insufficiency? and what is secondary adrenal insufficiency affect?

A

Primary—>something wrong with the adrenal glands

Secondary—>something wrong with the AP—>low ACTH—>low cortisol, not affect aldosterone

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25
Q

2 main causes of secondary adrenal insufficiency?

A

Iatrogenic/hypopituitarism

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26
Q

What causes the hyperpigmentation in primary adrenal insufficiency?

A

High ACTH level

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27
Q

Signs of acute adrenal insufficiency?

A

HoTN/nausea/vomitting/hyperkalemia (no aldosterone)/hyponatremia (increased ADH)

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28
Q

What drug is used to test for adrenal insufficiency?

A

Cosyntropin—>ACTH analog—>look for cortisol level

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29
Q

How do you treat chronic primary adrenal insufficiency?

A

Cortisol/aldosterone replacement maintenance

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30
Q

How to treat acute adrenal crisis?

A

IV fluid/high dose glucocorticoid (dexa or hydro)

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31
Q

What to do when pt with adrenal insufficiency is ill?

A

Increase dose of glucocorticoid

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32
Q

Treatment resistance HTN with hypokalemia, think?

A

Primary aldosteronism

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33
Q

How to diagnose 21-hydroxylase deficiency?

A

Cosyntropin—>increase 17-OH pregnenolone

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34
Q

Treatment for 21-hydroxylase deficiency?

A

Steroids (also suppress ACTH—>suppress androgen production)

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35
Q

What are the 2 toxicity of steroids?

A

Cushing’s syndrome/adrenal insufficiency with sudden withdraw

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36
Q

Thyroid produces which 3 hormones and where are they produced?

A

T3, T4 and calcitonin/colloid

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37
Q

How does iodide transported inside of colloid and what maintains the gradient?

A

I-Na symporter/Na K pump maintains the gradient

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38
Q

What do enzymes D1 and D2 do and where are they found?

A

Convert T4 to T3
D1: liver and kidney
D2: anywhere else

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39
Q

What does the enzyme D3 do?

A

Inactivate T3

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40
Q

What is the key enzyme in thyroid hormone production?

A

Thyroid peroxidase

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41
Q

How is thyroid hormone transported from colloid to blood?

A

endocytosis—>endosome—>fuse with lysosome—>release free thyroid

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42
Q

How does goiter occur in hypothyroidism?

A

TSH level increase—>thyroid size increases

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43
Q

Which population of pts need more dose of levothyroxine?

A

Infants and children

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44
Q

When do you need to readjust dosage for thyroid hormone replacement therapy?

A

4-6 weeks

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45
Q

What underlying disease should you be aware when given thyroid hormone replacement?

A

CAD/pregos—>need enough for fetal brain development

Both hyper and hypothyroidism causes birth defect

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46
Q

What is the mechanism of Grave’s disease?

A

Autoantibodies bind to TSH receptor on thyroid glands and produce thyroid hormone

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47
Q

What does nodular goiter produce?

A

Excessive amounts of thyroid hormones

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48
Q

Young pt with hyperthyroidism, what is the first treatment?

A

Anti thyroid drugs

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49
Q

What is the process of thyroxine production?

A

Tyrosine—(thyroid peroxidase)—>diiodotyrosine—(thyroid peroxidase)—>thyroxine

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50
Q

Which drug has lower risk for developing agranulocytosis, methimazole or propylthiouracil?

A

Methimazole

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51
Q

Which drug is used to treat hyperthyroidism in prego?

A

Propylthiouracil

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52
Q

How long does radioactive iodine need to start working?

A

Over 4 weeks

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53
Q

Why is radioactive iodine therapy contraindicated in prego and breast feeding pt?

A

Prego—>expose fetus to radiation

Breast feeding—>iodine pass into milk

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54
Q

What are cortical and trabecular bones?

A

Shafts of long bone/spine, ribs, pelves and etc.

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55
Q

40% of Ca is bound to?

A

Albumin

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56
Q

Hypercalcemia and PTH increases or decrease phosphorus excretion from the kidney?

A

Increase

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57
Q

The release of PTH needs which ion?

A

Mg2+

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58
Q

How does Vitamin D becomes active?

A

Become 25, OH Vit D in liver—>then become 125 (OH)2 Vit D in the kidney

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59
Q

What is the most common cause of primary hyperPTH?

A

Adenoma

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60
Q

What is the Ca/PTH/urine Ca level for familial hypocalciuric hypercalcemia?

A

Elevated Ca/normal PTH/low urine Ca

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61
Q

What is the normal serum Ca level?

A

8-10

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62
Q

Why do we use fluid to treat hypercalcemia?

A

To increase Ca excretion

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63
Q

What is the most common cause of secondary hyperPTH?

A

Renal disease—>phosphorus retention and low production of 125 (OH)2 D—>increase PTH

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64
Q

What causes tertiary hyperPTH?

A

Long standing secondary hyperPTH—>parathyroid gland become autonomous

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65
Q

What should you check first when see a low Ca level?

A

Albumin

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66
Q

What is the Ca and phosphorus level with Vit D deficiency?

A

Low Ca and phosphorus

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67
Q

Low phosphorus put pt in risk of ___ and ___?

A

Osteomalacia/rickets

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68
Q

What is the T score of bone density scan for osteoporosis?

A

Smaller than -2.5

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69
Q

How should biphosphonate being taken?

A

Take it first thing in the morning with empty stomach and full glass of water—>remain upright for 30mins

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70
Q

What catalyzes the formation of 1,25 (OH)2 D in the kidney?

A

1-alpha-hydroxylase

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71
Q

If PTH increase, 1-alpha hydroxylase increase or decrease?

A

Increase

72
Q

1-alpha hydroxylase is also called?

A

1,25 (OH)2 D

73
Q

Testosterone is converted to DHT by what enzyme in the peripheral?

A

5 alpha reductase

74
Q

What is the diagnostic value of HBa1c for DM?

A

over 6.5

75
Q

What is the legacy effect regarding DM?

A

Treat younger pt aggressively, even if they don’t control their blood sugar well later on, they still have fewer complications

76
Q

What is incretin and what is the most important incretin in human?

A

Incretin is secreted in the ileum and colon—>it stimulates insulin secretion
Glucagon like people 1 (GLP-1)

77
Q

What does GLP-1 do? and what is it metabolized by?

A

Stimulate insulin
promote fullness
suppress glucagon secretion
DPP-4

78
Q

GLP-1 is increased or decreased in type 2 DM?

A

Decreased

79
Q

Pt with risk of severe hypoglycemia should be prescribed ___? and what do you give in the hospital with this situation?

A

Glucagon injection/IV dextrose

80
Q

Reasons for oral DM therapy inadequacy?

A

Stress/diet/steroid usage

81
Q

How is detemir dosage dependent?

A

Low dose—>intermediate

High dose—>long lasting

82
Q

What is U-100 mean in terms of insulin con.?

A

100 units of insulin per mL

83
Q

Why is insulin secreted during fasting?

A

To counter glucagon and prevent ketone acidosis

84
Q

What’s the advantage of premixed insulin?

A

Longer shelf life/easier to use (mix long acting with intermediate or low)

85
Q

What’s the disadvantage of premixed insulin?

A

Unable to match carb intake or physical activity/

86
Q

When do we give insulin IV?

A

Give regular insulin for DKA

87
Q

Why injecting insulin in the ab region?

A

Most stable absorption

88
Q

What should the pt be taking caution when injecting regular insulin?

A

Regular insulin does not act right away—>might experience hypoglycemia after the meal

89
Q

Which kind of insulin is the least expensive?

A

NPH (intermediate)

90
Q

What would be a cheap program to manage DM? what is its disadvantage?

A

Regular insulin for breakfast/NPH for lunch/regular for dinner/NPH before bedtime
hypoglycemia at night

91
Q

What would be a more physiological approach to manage DM?

A

Use basal insulin (Glargine) daily and then fast acting for each meals

92
Q

How should the dosage insulin for each meal be determined?

A

Depends on how much carb is the pt eating

93
Q

What happens when a pt injects insulin at the same place?

A

Lipohypertrophy

94
Q

What kind of insulin is in the Continuous Subcutaneous Insulin Infusion (insulin pump)? and what is its advantage?

A

Fast acting/you can set basal rate and bolus

95
Q

The more the pt monitor their glucose level, the better or worse they manage their glucose level

A

Better

96
Q

Where do continuous glucose monitoring and finger pricking take the glucose level from?

A

Continuous: interstitial space (can be a lag)

Finger pricking: capillary

97
Q

which type of DM do the pt uses continuous glucose monitoring more often?

A

Type I

98
Q

What is the first line treatment for type I DM?

A

Basal bolus insulin therapy—>insulin pump/meal time insulin

99
Q

What tests should you run for pt with DM?

A

Lipid panel/kidney and liver function

100
Q

What else should you screen with type I DM?

A

Celiac

101
Q

Difference between primary and secondary adrenal insufficiency?

A

No hyperkalemia/hyperpigmentation for secondary

Hypoglycemia is more common in secondary

102
Q

What is the normal value of cortisol?

A

18-20 ug/ml

103
Q

What is ACTH stimulation test and what is it for?

A

Cosyntrophin (ACTH analog)—>cortisol level should increase normally—>exclude primary adrenal insufficiency/but can’t exclude secondary

104
Q

In what situation can ACTH stimulation test be given after steroid therapy?

A

If the steroid hasnt been given for a couple of days prior

If cortisol or cortisone were not given

105
Q

How to avoid HPA axis suppression with chronic therapy?

A

Use it less than 3 weeks/use alternate day therapy

106
Q

What is the effect of steroid on bones?

A

It can induce osteoporosis (Glucocorticoid induced osteoporosis)

107
Q

What kind of bone does steroid effect?

A

Trabecula bones

108
Q

How does glucocorticoid affects Ca absorption?

A

It inhibits intestinal Ca absorption and causes hypercalciuria

109
Q

What is glucocorticoid’s effect on leukocyte?

A

They inhibit leukocyte migration

110
Q

What is the mechanism of glucocorticoid on immunosuppressing?

A

Inhibit prostagland and leukotriene production/also inhibit COX 2

111
Q

Ketoconazole decreases the production of ___ and ___?

A

Androgen/cortisol

112
Q

What does thyroid peroxidase do?

A

It converts iodide into iodine

113
Q

Why PTU is recommended over methimazole during the 1st trimester of pregnancy?

A

PTU is more protein bound—>safer

114
Q

Insulin is increased by what 4 factors?

A

Glucose/sulfonylurea/M-agonist/beta 2 agonist

115
Q

Which receptor agonist would decrease insulin?

A

Alpha 2 agonist

116
Q

What kind of pt are more likely to develop lactic acidosis when taking metformin?

A

Pt with renal dysfunction or CHF

117
Q

What else Metformin can be used for besides DM?

A

PCOS to offset insulin resistance

118
Q

What does DPP-4 do?

A

Degrade GLP-1

119
Q

What does incretin do?

A

Secreted by small intestine—>increase insulin and decrease glucagon to lower glucose

120
Q

What does SGLT-2 do?

A

Located in proximal tubule to reabsorb glucose

121
Q

What drugs to give for diabetic neuropathy?

A

Gabapentin and TCAs

122
Q

Insulin promote or inhibit fatty acid synthesis in the liver?

A

Promotes

123
Q

What population is more prone to “Flatbush diabetes”?

A

Black/hispanic—>type II DM with DKA

124
Q

What is the triad for hyperosmolarity hyperglycemia state?

A

Hyperglycemia/hyperosmolarity/dehydration

125
Q

Which one has a higher level of serum glucose. DKA or HHS?

A

HHS (>600)

126
Q

How much glucose reduction per hour is the goal to correct DKA/HHS?

A

50-75 mg/dL/hr

127
Q

When do you give dextrose when managing DKA/HHS

A

when glucose comes down to 200-300

128
Q

Which one corrects faster, ketoacidosis or hyperglycemia?

A

Hyperglycemia corrects faster than ketoacidosis

129
Q

Why do we need to overlap IV and subQ insulin when the pt is coming out of DKA/HHS?

A

It takes subQ insulin 1-2 hours to start working

130
Q

What happens to intracellular K+ during acidosis?

A

K moves from intra to extracellular to try to buffer the blood—>K seems high—>but actually losing it through excretion—>hypokalemia (ventricular arrhythmia)

131
Q

What does insulin do to K?

A

It drives K back into the cell

132
Q

What ion value should you check before you start insulin for DKA/HHS pt?

A

K—>if low—>replenish K first and then start insulin

133
Q

When do we give bicarb to acidosis pt?

A

When pH is smaller than 6.5 (severe hyperkalemia)

134
Q

What would happen to K level when giving bicarb?

A

Hypokalemia

135
Q

What happens to the Na and phosphate level during DKA?

A

low

136
Q

Which ketone is the prominent one in DKA?

A

beta-hydroxy-butyric acid

137
Q

What happens to the level of beta-hydroxy-butyric acid/acetoacetic acid/acetone?

A

Beta-hydroxy-butyric acid is transformed to acetoacetic acid and then to acetone for excretion

138
Q

What value do we use to determine if the pt is out of DKA?

A

Closed anion gap/glucose7.3

139
Q

How do we know that the pt is out of HHS?

A

Normal osmolality/normal mental status

140
Q

What is the major complication upon correcting DKA?

A

Cerebral edema

141
Q

Which one has higher mortality, DKA or HHS?

A

HHS (elderly)

142
Q

What’s the formula for anion gap?

A

Na - (Cl + HCO3)

143
Q

What is normal anion gap?

A

12

144
Q

What is Winter’s formula? what does it measure?

A

PaCO2 = 1.5xHCO3 + 8+-2/evaluate respiratory compensation

145
Q

What does it indicate if the measured PCO2 is higher or lower than the calculated PCO2?

A

If measured is higher than the calculated—>additional respiratory acidosis
If measured is lower than the calculated—>additional respiratory alkalosis

146
Q

What is the rule of thumb for PaCO2?

A

Should be last 2 digits of pH

147
Q

What is the concept of delta delta?

A

When anion gap goes up by 1, bicarb drops by 1

In other words—>change in anion gap = change in bicarb

148
Q

What does it indicate if delta bicarb is greater or less than delta anion gap?

A

Greater—>anion gap acidosis + non anion gap acidosis (drive bicarb down)
Less—>anion gap acidosis + metabolic alkalosis (drive bicarb up)

149
Q

What is the triad of DKA?

A

Hyperglycemia/metabolic acidosis/high ketone

150
Q

What is the treatment approach for DKA?

A

Fluid and then insulin or K (check K level—>might have to give K before insulin)

151
Q

What is the formula for osmolality?

A

2xNa + urea/2.8 + glucose/18

152
Q

What would cause decompensation?

A

Infection/infarct/insulin

153
Q

What are essentials for dialysis?

A

Semipermeable membrane/anticoagulant

154
Q

What is the process of peritoneal dialysis?

A

Infusion of balanced salt solution with dextrose—>let it sit—>toxin diffuses across the peritoneal membrane—>drain it out

155
Q

How does AV fistula work?

A

Dilate vein for insertion of dialysis

156
Q

Drug dosing formulas are only useful for ___ renal function

A

Stable

157
Q

Pt with end stage renal disease (dialysis) need to restrict what intake?

A

Fluid (kidney can’t put out urine)/sodium/potassium/phosphate

158
Q

What are the hormone imbalance seen in end stage renal disease pt?

A

Low EPO/high PTH/low Vitamin D (decrease 1 alpha hydroxylase)

159
Q

What are the symptoms of uremia?

A

Loss of appetite/nausea/metallic taste/serositis (pericarditis)

160
Q

What are the factors that contribute to whether a drug should be replaced after dialysis?

A

Size (if small)/volume of distribution (if in blood)/no protein bound/duration of dialysis

161
Q

Besides phosphate restricting, what else should be given with dialysis pt?

A

Phosphate binders

162
Q

Should dialysis pt restrict protein intake?

A

No, encourage protein intake prevent malnurishment

163
Q

What formula is used for dose adjustment for end stage renal disease pt?

A

Cockcroft gault formula

164
Q

When do you start giving maintenance drugs for kidney transplantation?

A

Days after kidney starts to work

165
Q

How is the dose for cyclosporin and tacrolimus?

A

High level in the first month and then taper over the next 2 months

166
Q

How should mTOR inhibitors be dosed?

A

High dose early and lower dose later

167
Q

What are 2 drugs that might increase tacrolimus level?

A

Diltiazem/fluconazole

168
Q

Azathioprine interacts with what drug?

A

Allopurinol

169
Q

TZD is contraindicated in pt with what condition?

A

CHF

170
Q

All oral diabetic medications are contraindicated in what population? What to use instead?

A

Pregos/insulin injection

171
Q

If a pt is on glargine daily and lispro for dinner, what is determining her glucose level when she wakes up the next morning, glargine or lispro?

A

Glargine

172
Q

What 2 kinds of oral diabetic medications should not be used together?

A

Sulfonylurea and meglitinide

173
Q

High Ca and low phosphorus indicates? How?

A

Excess PTH/High PTH—>high Ca—>bind to more phosphorus—>low phosphorus

174
Q

What’s the difference between PTU and methimazole?

A

PTU additionally block the peripheral conversion of T4 to T3

175
Q

Which drug has higher chance of causing agranulocytosis, PTU or methimazole?

A

PTU

ESUN MS2Unit5 (4 decks)

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