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Endo Repro Midterm > Endo-Repro CIS > Flashcards

Endo-Repro CIS Flashcards

1
Q

What are the manifestations of short-term stress response?

A
  1. glycogen broken down to glucose; increased blood glucose
  2. increased BP
  3. increased RR
  4. increased metabolic rate
  5. change in blood-flow patterns, leading to increased altertness and decreased kidney activity
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2
Q

What are manifestations of acute adrenal insufficiency?

  • signs/symptoms
  • lab abnormalities

LO1

A

low BP
low RR
low metabolic rate
LOC

  • hypoglycemia
  • hyponatremia “salt wasting”
  • hyperkalemia
  • fever
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3
Q

Effect of primary adrenal cortical insufficiency on HPA

LO2a

A

low mineralcorticoids, low glucocorticoids – no negative feedback –> high ACTH

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4
Q

Effect of primary adrenal cortical insufficiency on renin-angiotensin II-aldosterone system

LO2b

A

low aldosterone – no negative feedback –> high renin and high angiotensin II

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5
Q

What is the pathology that underlies most cases of chronic adrenal insufficiency?

LO3

A

autoimmune
Addison’s disease
-chronic progressive destruction of adrenal gland
-high ACTH but low cortisol
-adrenal response is blocked from the signal

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6
Q

What are potential etiologies for acute adrenal insufficiency?

LO4

A
  • underlying Addison’s disease (flare)

- trauma

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7
Q

Describe the processes by which the parathyroid glands regulate calcium homeostasis

LO5

A

chief cells secrete PTH

  • directly releases calcium from bone
  • promotes synthesis of 1,25 (OH)2 D in the kidney –> vit D promotes calcium absorption from GI
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8
Q

Primary hyperparathyroidism

  • clinical presentation
  • labs
  • abnormalities

LO6a,b,c

A

clinical presentation
-hypercalciuria kidney stones
-increased bone resorption – brittle bones
-constipation
-neural symptoms
“stones, bones, groans, thrones, with neural undertones”

labs

  • elevated Ca2+
  • decreased Pi
  • elevated PTH
  • decreased urine Ca2+
  • elevated urine Pi –> phosphaturia

abnormalities

  • abnormality within parathyroid gland - 1 gland enlarged
  • parathyroid adenoma (tumor) secreting excess PTH
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9
Q

Secondary hyperparathyroidism

  • clinical presentation
  • labs
  • abnormalities

LO6a,b,c

A

clinical presentation

  • back pain
  • same as hypocalcemia: hyperreflexia, spontaneous twitching, muscle cramps, tingling, numbness

labs

  • decreased or normal Ca2+
  • elevated Pi
  • elevated PTH

abnormalities

  • ESRD–>low calcium–>elevated PTH–>increased bone turnover
  • vit D deficiency
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10
Q

Describe the progression of disease in the most common cause of secondary hyperparathyroidism.
-measure to arrest the disease process

LO7a

A
  • ESRD–>low calcium–>elevated PTH–>increased bone turnover
  • calcium supplement, if vit D levels decreased add vit D supplement
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11
Q

Pathophysiology of T1DM

  • etiology
  • hormone abnormality
  • effect on cell metabolism

LO8

A
  • autoimmune disease due to failure of T lymphocyte self tolerance
  • directed against beta cells
  • “insulinitis”
  • low insulin
  • insulin is anabolic –> catabolic cell metabolism in T1DM
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12
Q

T1DM

  • clinical signs and symptoms
  • labs

LO9

A 
polydypsia, polyuria
-excess sugar in bloodstream pulls fluid from tissues
extreme hunger
-insulin is unavailable, so sugar not moved into cells --> muscles and organs lack energy
weight loss
-muscle tissues and fat stores shrink
fatigue
-no sugar for cells
irritability or behavior changes
  • increased glucose
  • decreased insulin –> check for c peptide
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13
Q

DKA
-clinical signs/symptoms

LO10

A 
fruity smelling breath
-break down fat producing ketones
abdominal pain
-metabolic acidosis --> labored breathing
nausea/vomiting
  • increased blood glucose
  • high ketoacids in the liver
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14
Q

Thyroid goitrogenesis

-causes

A 
nutrition
-iodine deficiency
-goitrogens
genetics
-familial predisposition
environment
-alcohol
-smoking
-obesity/insulin resistance
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15
Q

Thyroid goitrogenesis
-pathophysiology

LO11

A

more thyroid cells needed to produce the same amount of thyroid hormone needed

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16
Q

Primary hyperthyroidism

  • clinical manifestations
  • labs

LO12a

A

clinical manifestations

  • increased BMR: muscle wasting, increased appetite
  • wt loss
  • heat intolerance
  • cardiac effect: tachycardia, palpitations
  • nervousness, excitability, restlessness, emotional instability, insomnia
  • SOB
  • diarrhea
  • exophthalmos
  • goiter (may have thrill and bruit)
  • periorbital edema

labs

  • increased free T3, T4
  • decreased TSH
  • presence of TSI
17
Q

Primary hypothyroidism

  • clinical manifestations
  • labs

LO12b

A

clinical manifestations

  • mental and physical sluggishness
  • wt gain
  • cold intolerance
  • cardiac effect: low CO
  • dry brittle hair
  • edema of face and eyelids
  • thick tongue, slow speech
  • deep, coarse voice
  • enlarged heart
  • diastolic hypertension

labs

  • low free T3, T4
  • TSH dependent on cause: hashimoto’s high, pituitary abnormality low
  • antithyroid antibody present if hashimotos thyroiditis
18
Q

Euthyroid goiter with mass effect

  • clinical manifestations
  • labs

LO12c

A

clinical manifestations

  • dysphagia
  • can’t breath when supine
  • diffusely enlarged, multinodular thyroid gland
  • no wt change

labs

  • TSH: normal
  • free T4: normal
  • T4: normal
19
Q

Euthyroid goiter

  • treatment indications
  • treatment options

LO13

A

obstructive symptoms

  • dysphagia
  • dyspnea

risk of malignancy

  • relative increased risk
  • difficult to follow for possible future development

treatment option

  • surgery
  • radioactive iodine therapy
20
Q

Pituitary somatotroph adenoma

  • clinical manifestations
  • diagnosis

LO14a

A

clinical manifestations: acromegaly

  • prominent supraorbital ridges
  • lower teeth separation
  • prominent lower jaw
  • cardiomegaly
  • large hands
  • organomegaly
  • hyperglycemia
  • accelerated osteoarthritis
  • large feet
  • mental disturabances
  • large head circumference
  • HTN

diagnosis

  • serum levels of IGF-1 elevated
  • oral glucose tolerance test for GH response
21
Q

pituitary corticotroph adenoma

  • clinical manifestations
  • diagnosis

LO14b

A

clinical manifestations
-cushing disease

diagnosis
-elevated ACTH

22
Q

pituitary thyrotroph adenoma

  • clinical manifestations
  • diagnosis

LO14c

A

clinical manifestations
-secondary hyperthyroidism

diagnosis

  • elevated TSH
  • elevated free T4
  • elevated T3
23
Q 
pituitary adenoma with mass effect
-clinical manifestations
-diagnosis
-treatment
LO14d
A

clinical manifestation

  • optic nerve compression: blurred vision, loss of visual fields
  • elevated intracranial pressure: HA, N/V

diagnosis
-CT/MRI

treatment
-surgery

Endo Repro Midterm (12 decks)

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