Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Drugs- Basic High Yield Stuff for Boards > Endo > Flashcards

Endo Flashcards

1
Q

treatment for prolactinoma MOA

A

Dopamine agonists (like bromocriptine/cabergoline)

or transsphenoidal resection

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

Adverse effect of anti-psychotics on prolactin

A

increase prolactin secretion (most anti-psychotics work via antagonizing dopamine)

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

treatment for Acromegaly/ Gigantism (2)

A
  1. somatostatin analogs (like Octreotide)

2. GH-R antagonist (pegvisomant)

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

treatment for central DI and nocturnal enuresis

A

desmopressin (ADH analog)

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

enzymes inhibited by Propylthiouracil

A
  1. thyroid peroxidase

2. 5’ deiodinase

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

enzyme inhibited by methimazole

A

thyroid peroxidase

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

Which endocrine hormones signal through cAMP? (12)

A

“FLAT ChAMP + cal+GHRH+glucagon”

  1. FSH/LH/TSH/hCG (these are all derived from same molecule)
  2. ACTH/CRH
  3. ADH(V2-R)
  4. MSH
  5. PTH/calcitonin
  6. GHRH
  7. Glucagon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which endocrine hormones signal through cGMP? (2)

A

“BAD GraMPa” (GraMPa=GMP)

  1. BNP/ANP
  2. E’D’RF (NO)
  • think vasodilators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which endocrine hormones signal through IP3 (Gq)? (7)

A

“GOAT HAG”

  1. GnRH
  2. Oxytocin
  3. ADH (V1-R)
  4. TRH
  5. Histamine (H1-R)
  6. Angiotensin II
  7. Gastrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which endocrine hormones have intracellular receptors? (7)

A

“PET CAT on TV”

  1. Progesterone
  2. Estrogen
  3. Testosterone
  4. Cortisonl
  5. Aldosterone
  6. T3/T4
  7. Vit D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which endocrine hormones signal via Receptor tyrosine kinase? (5)

A

Think growth factors (MAP-kinase pathway)

  1. Insulin
  2. IGF-1
  3. FGF
  4. PDGF
  5. EGF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which endocrine hormones signal via Non-receptor tyrosine kinase? (6)

A 
JAK/STAT pathway
"PIGGlET"
1. Prolactin
2. Immunomodulators (cytokines, IL-2, IL-6, IFN)
3. GH
4. G-CSF
5. Erythropoietin
6. Thrombopoietin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

treatment for Pheochromocytoma?

MOA

A

Phenoxybenzamine (also has 16 letters like Pheo)
- irreversible a-antagoist

Follow this with a BB prior to tumor resection

  • Never BB before a-angtagonist (always in alphabetical order) to avoid Hypertensive crisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

treatment for Thyroid Storm? (4)

A

Treat with the 4P’s

  1. BB (propranolol)
  2. Propylthiouracil
  3. Prednisone (decreases conversion of T4–>T3)
  4. Potassium iodine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

treatment for central DI? (2)

A
  1. desmopressin

2. hydration

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

treatment of nephrogenic DI? (5)

A
  1. hydrochlorothiazide (thiazide diuretic)
  2. indomethacin (NSAID= decrease renal flow)
  3. amiloride (K-sparing)
  4. hydration
  5. remove offending agent (like lithium)
  • scare body with volume depletion to cause increase proximal tubule saline reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of SIADH ?

A
  1. fluid restriction
  2. salt tablets
  3. IV hypertonic saline
  4. diuretics
  5. conivaptan
  6. tolvaptan
  7. demeclocyline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

treatment for Hypopituitarism?

A

Hormone replacement

corticosteroids, thyroxine, sex steroids, HG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

treatment for Diabetic ketoacidosis?

A

IV fluids
IV insulin
K to replace intracellular stores
Glucose as necessary to prevent hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Treatment of hyperosmolar hyperglycemia non-ketotic syndrome?

A

aggressive IV fluids

insulin therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

treatment for glucagonoma

A

ocreotide or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

treatment of insulinoma

A

surgical resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

treatment for somatostatinoma

A
  1. surgical resection

2. somatostatin analog (octreotide) for symptom control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

treatment for carcinoid syndrome

A
  1. surgical resection

2. somatostatin analog (octreotide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

treatment for Zollinger-Ellison syndrome

A

PPi or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

treatment STRATEGIES for Type1 DM (2)

A
  1. low carb diet

2. insulin replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

treatment STRATEGIES for Type2 DM (4)

A
  1. dietary modification and exercise for weight loss
  2. oral agents
  3. non-insulin injectables
  4. insulin replacementq
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

treatment STRATEGIES for Gestational DM (2)

A
  1. dietary modification and exercise

2. insulin replacement if lifestyle modification fails

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Rapid-acting insulin:

Name 3

A

“LAG”

  1. lispro
  2. aspart
  3. glulisine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Rapid-acting insulin:

MOA (liver, muscle, fat)

A

-binds Insulin-R rapidly
Liver: increase glycogen stores
Muscle: increase glycogen, increase protein synth, increase K+ uptake
Fat: increase TG storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Rapid-acting insulin:
Clinical Use
Risk/Concerns

A

Use: type 1, type 2, Gestational DM
(postprandial glucose)

  1. hypoglycemia
  2. lipodystrophy/ weight gain
  3. hypersensitivity rxn (rare)
32
Q

Short acting Insulin:
Alternative name
Clinical use (4)

A

Regular Insuline

Use:

  1. Type 1, type 2, Gestational DM
  2. DKA (IV)
  3. hyperkalemia (+ glucose)
  4. stress hyperglycemia
33
Q

Intermediate acting Insulin:
Alternative name
Clinical use

A

NPH

Use: Type 1, type 2, Gestational DM

34
Q

Long-Acting Insulin:
Name (2)
clinical use

A

Detemir and Glargine

Use: Type 1, type 2, Gestational DM (basal glucose control)

35
Q

Metformin:
Class
MOA

A

Biguanide

  1. decrease gluconeogenesis
  2. increase glycolysis
  3. increase peripheral glucose uptake/insulin sensitivity
36
Q

Metformin:
Admin
Clinical Use
Adverse

A

Oral
-Type 2 DM (first line, also causes weight loss)
(can be used in pt w/o islet function

  1. GI upset
  2. lactic acidosis (contra in Renal insufficiency)
37
Q

Sulfonylureas:
Name 1st generation (2)
Name 2nd generation (3)

A

First gen: 1. chlorpropamide 2. tolbutamide
Second gen: “lots of ‘G’s’”
1. glimepiride 2. glipizide 3. glyburide

38
Q

Sulfonylureas:
MOA
Clinical Use (1)

A
  • close K+ channels in Beta-cell membrane–> cell depot–> insulin release via increase Ca+2
  • stimulate release of endogenous insulin

Use: Type 2 DM (requires some islet function)

39
Q

Sulfonylureas:

Adverse (4)

A
  1. hypoglycemia (esp. in renal failure)
  2. weight gain

First gen: disulfiram-like Rxn
2nd gen: hypoglycemia

40
Q

Glitazones/Thiazolidinediones:
Name (2)
MOA

A
  1. Pioglitazone
  2. Rosiglitazone

increase insulin sensitivity in peripheral tissue via binding PPAR-g nuclear transcription regulator

41
Q

Glitazones/Thiazolidinediones:
Clinical Use
Adverse

A

Mono or combo in Type2 DM
**SAFE IN RENAL IMPAIRMENT

  1. Weight gain/edema
  2. Hepatotox
  3. Heart failure
  4. increase risk of fractures
42
Q

Should patients with renal failure use Metformin?

A

NO

43
Q

Meglitinides:
Name 2
MOA

A
  1. Nateglinide
  2. Repaglinide

Stimulate postprandial insulin release via binding K+ channels on Beta-cells (site differ from sulfonylureas)

44
Q

Meglitinides:
Clinical Use
Adverse (2)

A

Monotherapy or w/ Metformin in Type2 DM

  1. Hypoglycemia (increase with renal failure)
  2. weight gain
45
Q

GLP-1 analogs:
Name 2. Which is SC injection?
MOA (4)

A 
1. Exenatide
2 Liraglutide (sc injection)

increase glucose-dependent insulin release
decrease glucagon release
decrease insulin gastric emptying
increase satiety

46
Q

GLP-1 analog:
Clinical Use
Adverse (3)

A

Type 2 DM

  1. N/V
  2. Pancreatitis
  3. modest weight loss
47
Q

DPP-4 inhib:
Name 3
MOA

A
  1. Linagliptin
  2. Saxagliptin
  3. Sitagliptin

inhib DPP-4 enzyme that deactivates GLP-1 –>
increase glucose-dependent insulin release
decrease glucagon
decrease gastric emptying
increase satiety

48
Q

DPP-4 inhib:
Clinical Use
Adverse (1)

A

Type 2 DM

1. Mild urinary or respiratory infections
weight neutral

49
Q

Amylin analogs:
Name 1. Admin
MOA

A

Pramlintide (SC injection

decrease gastric emptying
decrease glucagon

50
Q

Amylin analogs:
Use
Adverse(2)

A

Type 1 & Type 2 DM

  1. Hypoglycemia (in setting of mistimed prandial insulin)
  2. N/D
51
Q

Sodium-glucose Co Transporter 2 Inhib (SGLT-2):
Name 3
MOA

A
  1. Canagliflozin
  2. Dapagliflozin
  3. Empagliflozin

Block reabsorption of Glucose in PCT

52
Q

SGLT-2:
Clinical Use
Adverse (4)

A

Type 2 DM

  1. Glucosuria
  2. UTIs/ vaginal yeast infections
  3. hyperkalemia
  4. dehydration (orthostatic hypotension)
53
Q

a-glucosidase inhib:
Name 2
MOA

A
  1. Acarbose
  2. Miglitol

inhib intestinal brush-border a-glucosidase
delayed Carb hydrolysis and glucose absorption –>decresae postrandial hyperglycemia

54
Q

a-glucosidase inhib:
Clinical use
Adverse(1)

A

Type 2 DM

  1. GI disturbance
55
Q

Thionamides:

Name 2

A
  1. Propylthiouracil (PTU)

2. Methimazole

56
Q

Thionamides:

MOA

A

Both block Block thyroid peroxidase
–inhib oxidation of Iodide & organification/coupling of iodine–>inhib thyroid hormone synthesis

Propylthiouracil also blocks 5’-deiodinase–>decrease peripheral conversion of T4-to-T3

57
Q

Thionamides:
Clinical use / which is safe in pregnancy?
Adverse

A
  1. Hyperthyroidism
  2. PTU=Pregnancy (methimazole= aplasia cutis teratogen)

Adverse:

  1. Skin rash
  2. Agranulocytosis (rare)
  3. aplastic anemia
  4. hepatotox
58
Q

Levothyroxine mimics

A

T4

59
Q

Triiodothyronine mimics

A

T3

60
Q

Levothyroxine/Triiodothyronine:
MOA
Clinical use (3)
Adverse (4)

A

MOA: thyroid hormone replacement
Use: 1. Hypothyroidism 2. Myxedema 3. Weight loss supplement (off label)

Adverse: Tachycardia, Heat intolerance, tremors, arrhythmias

61
Q

Conivaptan and Tolvaptan:
MOA
Clinical Use

A

ADH antagonists

  1. SIADH (block action of ADH at V2-R)
62
Q

Demopressin:

Clinical use

A

Central DI

63
Q 
GH:
clinical use (2)
A
  1. GH deficiency

2. Turner syndrome

64
Q 
Oxytocin:
Clinical use (3)
A
  1. stimulates labor/ uterine contractions
  2. control uterine hemorrhage
  3. milk-let down
65
Q 
Somatostatin analog (octreotide): 
Clinical use (5)
A
  1. acromegaly
  2. carcinoid syndrome
  3. gastrinoma
  4. glucagonoma
  5. esophageal varices
66
Q

Demeclocycline:
MOA
Clinical Use
Adverse (3)

A 
ADH antagonist (member of tetracycline family)
Tx: SIADH

Adverse:

  1. Nephrogenic DI
  2. Photosensitivity
  3. Abnorm Bone/teeth
67
Q

Glucocorticoids:

Name 6

A
  1. Beclomethasone
  2. Dexamethasone
  3. Hydrocortisone
  4. Mehtylpredisolone
  5. Prednisone
  6. triamcinolone
68
Q

Glucocorticoids:

MOA

A 
Metabolic/catabolic/anti-inflam/immunosuppressive
mediated by: 
1. glucocorticoid response elements
2. inhib phospholipase A2
3. inhib NF-kB
69
Q 
Glucocorticoids:
Clinical Use (4)
A
  1. Adrenal insuff/ Addison/ Cong. adrenal hyperplasia
  2. inflamm
  3. immunosuppression
  4. asthma/allergies
70
Q

Glucocorticoids:

Adverse (6)

A
  1. Iatrogentic Cushings
  2. Adrenal insuff when abruptly discontinued after chronic use
  3. adrenocortical atrophy
  4. peptic ulcers
  5. steroid diabetes
  6. steroid psychosis cateracts
71
Q

Signs/Symp of Cushings

A
  1. hypertension
  2. weight gain/moon face/truncal obesity, buffalo hump
  3. thinning of skin, striae
  4. acne/amenorrhea
  5. hyperglycemia
  6. osteoporosis
  7. immunosuppression
72
Q

Fludrocortisone:
MOA
Clinical Use
Adverse

A
  • Synthetic analog of aldosterone w/ little glucocorticoid effects
  • Use: Mineralocorticoid replacement for primary adrenal insuff
  • Adverse: like glucocorticoids (edema/HF/hyperpigmentation)
73
Q

Cinacalcet:
MOA
Clinical Use
Adverse

A
  • sensitizes Ca+2 sensing receptor in parathyroid gland to circulating Ca+2–> decrease PTH
  • primary/secondary hyperPTH
  • Hypocalcemia
74
Q

treatment for Turner Syndrome

A

GH

75
Q

Which DM drugs cause Weight gain?

A
  1. insulin
  2. Sulfonylureas (both generations)
  3. Glitazones/Thiazolidinediones
  4. Meglitinides

Drugs- Basic High Yield Stuff for Boards (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions