Drugs Flashcards

1
Q

Somatropin (admin?)

A

= Growth Hormone

SC (or IM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mecasermin

A

Recombinant IGF-1 (SC and have carbs before to avoid hypoglycemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tesamorelin (admin and ADR)

A
GHRH analog (IV, nasal, SC)
ADR: face flushing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Ocreotide (& admin)

A

Somatostatin analog (IM or SC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Effect of ghrelin?

A

Causes GH release! (like GHRH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lanreotide

A

Somatostatin analog (SC) longer acting than ocreotide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Somatostatin and analogs ADR?

A

Drops glucose tolerance so hyperglycemia

AND sinus bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pegvisomant

A

GH-R antagonist (SC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cabergoline

A
Preferred DA (D2) agonist (inhibits GH secretion??? AND INCREASES inhibition on PRL so decreases PRL release)
ALSO USED FOR CUSHINGS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bromocriptine

A

DA agonist

FREQUENT SIDE EFFECTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Quinagolide

A

DA agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
Side effect of anti-psychotics
(and other class of drugs with same side-effects?)
A

Blocks D2 receptors in Hypothalamus, so can produce prolactinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ADH

A

= Vasopressin (released in response to rising blood osm and decreasing blood volume)
Helps concentrate urine, via GPCR
Can be inhibited by ethanol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

DDAVP (aka Desmopressin)

A

ADH analog (more stable to degradation than ADH -longer half-life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Roles of ADH

A

Renal: V2 –> Gs
(increases aquaporins and increases urea and Na+ transporters)
Non-renal V2 (still –> Gs): release of coag factor VIII and von Willebrand
Vasonconstriction: (At much higher Cp) V1 –> Gq, constricts vascular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Central DI (inadequate ADH secretion)

A
Give DDAVP (aka Desmopression)
And if intolerant give chlorpropamide
17
Q

Nephrogenic (inadequate DI actions)

A

Give thaizide diuretics and NSAIDS

18
Q

SIADH (too much ADH)

A

leads to hyponatremia
Give demeclocyline (blocks ADH action in cascade)
Or V2 receptor agonists Tolvpatan, Conivaptan
ALSO give 3% NaCl

19
Q

If hyponatremia corrected too quickly you get ..

A

cerebellar pontine myelinolysis

20
Q

Aldosterone Antagonists?

A

Spironolactone, Epleperone
Give for APA/IHA (i.e PRIMARY ALDOSTERONISM)
IHA with BP meds too
Cannot screen for APA/IHA if already on these drugs

21
Q

Drugs that cause Hypothryroidism?

A

Lithium, Amiodarone, Cholestyramine, Phenytoin, Carbamazepine
LAC and the PC anti-convulsives (that decreae TBG binding)

22
Q

When to treat hypothyroid? With what? and the risks?

A

when TSH >10, with levothyroxine (T4) and the big risk is CVD - it has narrow therapeutic range AND SYMPATHETIC OVERACTIVTY (so beware anticongestants)

23
Q

DDIs that impair Levothryroxine absorption?

A

cipro, BILE ACID SEQUESTRANTS, raloxifane, sucralfate

24
Q

Drugs that block/inhibit 5’deidoidinase?

A
glucocorticoids
B-blockers
AMIODARONE
And high doses of PTU (propothiouracil)
Also effected by malnutrition, illness, fetal/neonatal period
25
Q

Myxedema Coma (sx and treatment)

A

drop in CO, bradycardia, HYPOTHERMIA, low NA and low GLU

GIVE Large does of T4 and hydrocortisone to prevent and adrenal crisis

26
Q

Levothyroxine time to improvment?

A

6-8 weeks

27
Q

Liothyronine

A

synthetic T3

28
Q

Liotrix

A

mix of T4 and T3, not rec

29
Q

Liothyronine (T3) vs Levothyroxine (T4)

A
shorter half life 
greater oral bioavailability
greater affinity for TH-R receptor (10x)
higher cost
may increase osterporosis risk
greater risk of cardio tox
30
Q

Thyroid Storm treatment?

A
A-FIB, ans SUPERHYPERTHYROID, 
Give PTU (blocks T4-->T3), Propanolol (sx and blocks T4-->T3) and NaI or KI
31
Q

Methimazole vs PTU

A

for hyperthyroid (so first line Graves and FU with B-blocker)
Mech: a thionamide that inhibits TPO
Methimazole is QD compared to PTU that is TD
PTU is T4–>T3 blocker and PREFERRED in PREG, but also has liver probs assoc.
PTU has a longer half life, but METH is lower dose and more rapid to work
BOTH RESOLVE IN 2 WEEKS

32
Q

Graves recurrence

A

60-70%

33
Q

Methimazole and PTU most dagerous side effect

A

agranulatomous cytosis - WBC count drops esp. neutrophils

34
Q

Ketoconazole

A

Cortisol synth inhib

for CUSHINGS

35
Q

ACTH secretion inhib

A

Cabergoline (D2 agonist)

Pasireotide (SST analog)

36
Q

Mitotane

A

Adrenolytic Agent

CUSHINGS

37
Q

Mifepristone

A

Cortisol Receptor Blocker

CUSHINGS

38
Q

Pheochromocytme treatment

A

a-blocker (-zosin)
THEN B-blocker
OR CCB alone
Then surgery