Brainscape's Knowledge GenomeTM

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


See full index

STEP > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is SIADH and what are the causes?

A 
Excess release of ADH from the neurohypophysis
Caused by:
1. Malignancies
- Small cell carcinomas
- Carcinoma of the pancreas
- Ectopic ADH secretion
2. Non-malignant pulmonary disease 
- TB
- Pneumonia
- Lung access
3. CNS disorders
- Head injury
- Cerebral vascular accident
- Encephalitis
4. Drugs
- Chlorpropramide
- Clofibrate
- Vincristine
- Vinblastine 
- Cyclophosphamide
- Carbamazepine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the clinical findings in SIADH?

A
  • Water retention and extracellular fluid volume expansion without edema or hypertension, owning to natriuresis
  • Hyponatremia results from water retention and sodium loss
  • Concentrated urine with Uosm > 300 most
  • Irritability, confusion, seizures and comma may result in severe hyponatremia ( < 120 mOsm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is SIADH diagnosed?

A
  • Hyponatremia <130 mEq/L and Posm <270 mOsm/kg
  • Urine sodium concentration >20 mEq/L (inappropriate natriuresis), maintained hypervolemia, suppression of renin-angiotensin system and no equal conc. of ANP
  • Low BUN, low creatinine, low serum uric acid and low albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is SIADH treated?

A

Fluid restriction to inder 1 L/d

Demeclocycline can be used

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

Type I Diabetes increases the risk of developing what other diseases?

A

Other autoimmune disorders such as Hashimoto thyroiditis and autoimmune adrenalitis (most common cause of primary adrenal insufficiency “addisons”)

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

Primary Adrenal Insufficiency

“ Addisons Disease”

A
  • Results from autoantibody against all 3 zones of the adrenal cortex
  • Exogenous ACTH does not increase serum cortisol
  • Increased ACTH due to loss of negative feedback from cortisol
  • MSH (melanocyte stimulating hormone) is a byproduct of ACTH production and is increased.
  • Deficiency of aldosterone and cortisol production
  • Lack of aldosterone decreases Na+ reabsorption and K+ and H+ excretion
  • Decrease in H+ excretion cause non-anion gap metabolic acidosis with low serum HCO3
  • Leads to compensatory Cl- retention to maintain electrical neutrality
  • Hypotension, (hyponatremic volume contraction), hyperkalemia, hyperchloremia, metabolic acidosis, skin and mucosal hyperpigmentation (due to increased MSH).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute Primary Adrenal Insufficiency

A
  • Sudden onset ( may be due to massive hemorrhage)
  • May present with shock in acute adrenal crisis
  • Waterhouse-Friderichsen Syndrome is usually due to an adrenal hemorrhage associated with septicemia from N. meningitidis, DIC or endotoxic shock.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Chronic Primary Adrenal Insufficiency

A
  • Usually due to adrenal atrophy or destruction by disease
  • Western world: autoimmune destruction
  • Developing world: Tuberculosis:
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Secondary Adrenal Insufficiency

A
  • Seen with decreased pituitary ACTH production
  • No skin/mucosal hyperpigmentation
  • No hyperkalemia (aldosterone synthesis is preserved from RAAs)
  • Labs show low cortisol and low ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Tertiary Adrenal Insufficiency

A
  • Seen in patients with chronic exogenous steroid use
  • Precipitated by abrupt withdrawal
  • Aldosterone synthesis is unaffected
  • Labs show low cortisol and low ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the typical symptoms seen in adrenal insufficiency?

A
  • Weakness
  • Fatigue
  • Orthostatic hypotension
  • Muscle aches
  • Weight loss
  • GI disturbances
  • Sugar/salt cravings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is adrenal insufficiency treated?

A
  • Glucocorticoid/mineral corticoid replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the metyrapone stimulation test?

A
  • Tests for adrenal insufficiency
  • Blocks the last step in cortisol synthesis
  • Blocks 11-deoxycortisol => cortisol
  • Normal response: shows decreased cortisol and increased ACTH and 11-deoxycortisol
  • Primary adrenal insufficiency: shows increased ACTH and decreased 11-deoxycortisol
  • Secondary adrenal insufficiency: shows decreased ACTH and 11-deoxycortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MEN type 1

A
  1. Parathyroid Adenoma (Primary Hyperparathyroidism)
    - Hypercalcemia
  2. Pituitary Endocrine Tumors
    - Prolactin, visual defects or GH
  3. Pancreatic Tumors
    - Gastrinoma (most common)
    - Zollinger Ellison syndrome
    - Insulinoma
    - VIPomas
    - Glucagonoma (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MEN Type 2A

A
  1. Medullary Thyroid Cancer
    - Neoplasm of parafolicular C Cells
    - Secretes calcitonin
    - Prophylactic Thyroidectomy Required
  2. Pheochromocytoma
    - Metanephrines
    - Headaches
    - Mutation in RET in cells of neural crest origin
  3. Parathyroid Hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MEN Type 2B

A
  1. Medullary Thyroid Cancer (Calcitonin)
  2. Pheochromocytoma
  3. Mucosal Neuromas / Marfinoid Habitus
    - Mutation in RET gene
17
Q

What is Marfinoid Habitus?

A
  • Tall and slender build with disproportionately long arms, legs and fingers
  • Found in MEN type 2B
  • Mutation in RET proto-oncogene
18
Q

Medullary Thyroid Carcinoma

A
  • Neoplasm that originates from parafollicular “C Cells”
  • Produces Calcitonin
  • Sheets of cells in an amyloid stroma (stains with congo red)
  • Associated with MEN 2A and 2B
  • RET mutations
  • Physical exam may show unilateral or bilateral thyroid mass
  • Diagnosed with fine needle aspiration
  • Treated with thyroidectomy
19
Q

What is an important predictor of insulin resistance?

A
  • Visceral obesity as measured by waist circumference or wist-to-hip ratio
  • ## Because excess visceral fat (surrounding internal organs) correlates more with insulin resistance than subcutaneous fat
20
Q

When do you start a patient with PCOS on metformin?

A

When their insulin levels are elevated

21
Q

17-Hydroxylase Deficiency

A
  • Impaired sex steroid and cortisol synthesis
  • Increased production of mineralcorticoids (aldosterone)
  • Females are born with normal genitalia
  • Males are born with ambiguous genitalia (undervirilized)
  • Affected individuals develop hypokalemia due to aldosterone excess
  • Do not undergo puberty (no sex steroids)
22
Q

21-Hydroxylase Deficiency

A
  • Decreased mineralocorticoid (aldosterone) and glucocorticoid (cortisol) synthesis
  • Increased adrenal androgen production
  • Females are born with ambiguous genitalia due to androgen excess
  • They frequently develop hypotension and hyperkalemia due to aldosterone deficiency.
23
Q

11-Hydroxylase Deficiency

A
  • Results in excessive androgen production
  • Result sin excess weak mineralocorticoid production (11-deoxycorticosterone
  • Leads to hypertension and hyperkalemia due to 11- deoxycorticosterone acting as aldosterone
  • Females are born with ambiguous genitalia (virilization)
24
Q

5Alpha-Reductase Deficiency

A
  • Results in ambiguous genitalia in males
  • Defective conversion of testosterone to dihydrotestosterone
  • Females have normal genitalia
  • Blood pressure and electrolytes are unaffected
25
Q

What is side-chain cleavage enzyme?

What does its deficiency lead to?

A
  • It is the first enzyme in the steroidogenic pathway
  • It converts cholesterol to pregnenolone
  • Deficiency leads to impaired synthesis of all steroid hormones
  • Complete deficiency is lethal due to absent placental progesterone synthesis
26
Q

Pheochromocytoma

pathogenesis?

A
  • Arises from neuroendocrine cells in adrenal medula
  • 25% are inherited
    1. VHL (von Hippel-Lindau)
    2. RET gene (multiple endocrine neoplasia type 2)
    3. NF1 gene (neurofibromatosis)
  • Symptoms result from increased catecholamine secretion
27
Q

What are the symptoms from a pheochromocytoma?

A
  • Headaches
  • Tachycardia/palpitations
  • Sweating
  • Hypertension (may be paroxysmal or persistent)
  • DIaphoresis
28
Q

What are the rule of 10s?

A

Pheochromocytoma

  • 10 % are bilateral
  • 10% are extra adrenal (paragangliomas)
  • 10% are malignant
29
Q

How to do you diagnose pheochromocytoma?

A
  • Elevated urinary and plasma catecholamines and metanephrines
  • CT scan
30
Q

What are the counterregulatory hormones that play a role in maintaining blood glucose levels?

A
  • Insulin secretion decreases leading to decreased peripheral glucose utilization and increase hepatic gluconeogenesis and glycogenolysis
  • Glucagon secretion increases leading to increased hepatic gluconeogenesis and glycogenolysis
  • Epinephrine secretion increases leading to increased hepatic gluconeogenesis and glycogenolysis
    and increased mobilization of gluconeogenic substrates
  • Increased cortisol and growth hormone leads to alteration of many genes to conserve glucose
31
Q

Out of all the counterregulatory hormones that maintain blood glucose levels, which has receptors located within the cytoplasm and translocate to the nucleus?

A

Cortisol

STEP (28 decks)

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