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Patho 2 > 1 - Endocrine Patho > Flashcards

1 - Endocrine Patho Flashcards

1
Q

Target cells may fail to respond to a hormone due to abnormalities in two places:

A

The cell surface receptors (most for water soluble hormones)

Inside the cell (abnormal second messengers

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2
Q

What types of medications may cause SIADH, especially in the elderly?

A

hypoglycemics

antidepressants

antipsychotics

narcotics

general anesthetics

cehmo

NSAIDs

synthetic ADH

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3
Q

Why is transient SIADH common after pituitary surgery?

A

All the stored ADH is released in an unregulated fashion

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4
Q

SIADH manifests as:

A
  1. hypoosmolar plasma (<280) with hyponatremia (<135)
  2. hyperosmolar urine
  3. urine sodium excretion equal to sodium intake
  4. normal adrenal/renal/thyroid function
  5. absence of other causatives (heart failure etc)
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5
Q

Treatment of SIADH includes:

A
  1. Underlying cause
  2. fluid restriction of 800-1000ml
  3. emergency correction of hyponatremia if symptomatic
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6
Q

How long does it usually take for SIADH to resolve?

A

3 days

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7
Q

What renal disorders can lead to nephrogenic DI?

A

pyelonephritis

amyloidosis

destructive uropathies

PKD

intrinsic renal disease

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8
Q

What drugs can result in a reversible nephrogenic DI?

A

lithium carbonate

colchicines

Ampho B

loop diuretics

general anesthesia

demeclocycline

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9
Q

What is gestational DI?

A

Rare pregnancy complication

level of vasopressinase is elevated

usually mild and doesn’t require treatment

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10
Q

Which has a more gradual onset: central or nephrogenic DI?

A

nephrogenic

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11
Q

Diagnostic criteria for DI are:

A

urine SG < 1.010

Urine Os < 200

Serum Os > 300

Hypernatremia

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12
Q

What is dipsogenic DI?

A

DI cause by excessive thirst and drinking

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13
Q

__________ is an ADH precusor molecule that can be used to measure ADH secretion

A

copeptin

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14
Q

What causes hypopituitarism? (3)

A
  1. Problem with the hypothalamus’ production of HRH
  2. Problem with the pituitary stalk cuts off comms
  3. AP gland can’t produce hormones
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15
Q

What is Sheehan Syndrome?

A

Postpartum hypopituitarism caused by a severe hemorrhage resulting in a pituitary infarction

Very rare

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16
Q

What is panhypopituitarism?

A

All the hormones of the AP are deficient

lack of cortisol from ACTH

lack of thyroid from TSH

lack of FSH AND LH

stunted growth from lack of GH

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17
Q

What are the s/s of ACTH deficiency?

A
  1. N/V, anorexia
  2. Fatigue and weakness
  3. Hypoglycemia d/t insulin sensitivity, decreased glycogen reserves and decreased gluconeogenesis
  4. Decreased aldosterone secretion
  5. Decreased GFR and urine output
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18
Q

What is myxedema

A

the characteristic sign of hypothyroidism

nonpitting, boggy edem in around the eyes, hands, and fett and supraclaviular fossae

Tongue and laryngeal and pharyngeal mucous membranes thicken

thick, slurred speech and hoarseness

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19
Q

Which is usually worse: primary hypothyroidism or TSH deficiency?

A

Primary

reduced TSH usually results in mild myxedema

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20
Q

What does a deficiency of LH and FSH cause?

A

amenorrhea

atrophy of the vagina, uterus, and breasts

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21
Q

How does GH deficiency manifest in children?

A

Hypopituitary dwarfism

Fasting hypoglycemia

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22
Q

How does GH deficiency manifest in adults?

A

increased body fat

decreased muscle

osteoporosis

reduced sweating, dry skin

psuch issues

MI from dyslipidemia and atherosclerosis

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23
Q

Hyperpituitarism is often caused by a ______

A

primary adenoma

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24
Q

What causes acromegaly?

A

Exces GH and IGF-1

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25
Q

Acromegaly is almost always caused by increased GH from:

A

a GH secreting pituitary adenoma

Almost never from ectopic production of GHRH

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26
Q

Why does elevated GH often lead to diabetes?

A

GH prevents peripheral glucose uptake, increases hepatic glucose production, and causes insulin resistance

The pancreas produces more insulin, but eventually insulin resistance and pancreatic exhaustion cause DM

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27
Q

What cardiac defects are seen in nearly 50% of patients with acromegaly?

A

HTN and L heart failure

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28
Q

Pituitary tumors that secrete _______ are the most common pituitary adenomas

A

prolactin

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29
Q

What kind of medications can increase prolactin?

A

Anything that decreases dopamine levels

risperidone

metoclopramide

TCAs

Methyldopa

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30
Q

How does excess prolactin manifest in men and women?

A

Hypogonadism

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31
Q

What causes postpartum thyroiditis?

A

pathologically related to Hashimoto disease

occurs 6-12 months after delivery

hyperthyroid phase precedes a hypothyroid phase

recover spontaneously 95% of the time

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32
Q

If there is a primary elevation in Thyroid Hormone, what will happen to TSH levels?

A

They will decrease

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33
Q

If there is a secondary elevation in Thyroid hormone, TSH levels will be:

A

elevated

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34
Q

Which is more common: primary hyperthyroidism or secondary hyperthyroidism?

A

Primary

the problem is usually with the thyroid, not the hypothalamus

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35
Q

50-80% of hyperthyroidism is caused by:

A

Grave’s Disease

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36
Q

Grave’s disease results from a type ______ hypersensitivity

A

Type II

Thyroid-Stimulating Immunoglobulins override normal negative feedback mechnaisms and cuase hyperplasia of the gland

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37
Q

The TSH in a patient with Grave’s disease would most likely be:

A

Low

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38
Q

What is pretibial myxedema?

A

lumpy and swollen red rash over the tibia from GRAVES DISEASE

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39
Q

What usually causes thyroid storm?

A

when people who have undiagnosed or uncontrolled hyperthyroidism are exposed to extreme stress from other causes (infection, trauma, burns, seizure, surgery, emotioanl distress, dialysis)

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40
Q

Describe the TSH levels for patients with:

primary hypothyroidism

secondary hypothyroidism

A

high

low

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41
Q

The most common cause of primary hypothyroidism is:

A

Hashimoto disease

(autoimmune thyroiditis)

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42
Q

How would the levels of TSH and TH appear in a patient with subclinical hypothyroidism?

A

TH would be normal

TSH would be elevated

43
Q

Describe the difference between the following types of hyperparathyroidism:

Primary

Secondary

Tertiary

A
  • primary*: increased PTH secretion, usually from parathyroid adenoma. Hypercalcemia, hypophosphatemia
  • Secondary:* incrased PTH in response to chronic hypocalcemia, usually due to CKD or Vitamin D deficiency
  • Tertiary*: develops after longstanding hypocalcemia d/t dialysis or GI malabsorption. Problematic after renal transplant, because the body is suddenly producing way more PTH than it actually needs
44
Q

Describe the effects of hyperparathyroidism on renal function

A

Causes hypercalcuria and hyperphosphaturia

Causes alkaline urine

Prediposed to calcium stones

impairs the concentraing ability of the renal tubule by decreasing its response to ADH

45
Q

The most common cause of hypoparathyroidism is:

A

surgical removal of the thyroid

46
Q

Hypo_______ inhibits PTH secretion

A

magnesemia

47
Q

What are the s/s of hypocalcemia?

A

perioral numbness, parasthesias, tingling, tetany

hyperreflexia

Chvostek’s (cheek) and Trousseau (BP cuff)

48
Q

What is the most common pediatrics chronic disease?

A

Type 1 DM

49
Q

When is DM1 usually diagnosed?

A

12 years old

50
Q

Both a lack of ______ and an excess of ______ contribute to DM1

A

insulin

glucagon

Alpha and beta cell functions are both abnormal. Amylin, which ordinarily inhibits glucagon, is also not produced

51
Q

Is the onset of Type 1 DM gradual or acute?

A

gradual

The later in life it starts, the longer the latent period usually is, so people who are near-adult are sometimes misdiagnosed with DM2

52
Q

Why is glucagon elevated in DM2?

A

pancreatic alpha cells become less responsive to glucose inhibition

53
Q

For a patient in DKA, describe the following labs:

BG

Bicarb

Anion Gap

A

>250

low

increased

54
Q

What is the most common precipitating factor for DKA?

A

Intercurrent illness: infection, trauma, surgery, MI

55
Q

What are the pathophysiology mechanisms for DKA?

A

Insulin deficiency is further antagonized by cortisol, glucagon, and GH released d/t stress

These hormones make insulin deficiency even worse

Results in decreased glucose uptake, increased fat mobilization, accelerated gluconeogenesis, glycogenesis, and ketogenesis

56
Q

Why does DKA cause a metabolic acidosis?

A

Everytime a ketone is formed, bicarb is lost

Normally the body uses ketones in tissues for energy, releasing that bicarb

But in the total absence of insulin, the liver produces ketones at a rate that exceeds peripheral use

these ketones eat up bicarb and accumulate

The ketones form strong organic acids that aren’t buffered by bicarb

57
Q

What are the criteria for diagnosis of DKA?

A
  1. serum glucose > 250
  2. Bicarb < 18
  3. pH <7.3
    • anion gap
  5. presence of urine and serum ketones
58
Q

Why is ketoacidosis only present in DM1?

A

Insulin has an anti-lipolytic effect

It moderates the rate at which the liver produces ketones in a high stress state

Without any insulin present, the lipolytic effect is completely unchecked, resulting in waaaay more ketones than the body could possibly use for energy

59
Q

Hyperglycemia likely induces mitochondrial:

A

overproduction of oxygen free radicals, leading to activation of the metabolic pathways known to cause atherosclerosis etc

60
Q

Why is hyperglycemia particularly hard on the kidneys, blood vessels, eyes, and nerves?

A

All these tissues don’t require insulin for glucose transport

That means in the setting of hyperglycemia, they can’t just downregulate the cellular uptake of glucose

Instead, it gets shunted into the polyol pathway for metabolism

Overactivation of polyol causes excess sorbitol (swelling) and reduced glutathione (an antioxidant)

61
Q

Many of the microvascular complications of hyperglycemia are likely due to inappropriate activation of which signalling pathway?

Why?

A

DAG - Protein Kinase C

Once activated, PKC may cause insulin resistance, cytokine production, vascular proliferation, enhanced contractility, angiogenesis, and increased permeability

62
Q

What is glycation?

A

the nonenzymatic, reversible binding of glucose to proteins, lipids, and nucleic acids

63
Q

How is glycation altered in recurrent/persistent hyperglycemia?

A

glucose becomes irreversibly bound to collagen and other proteins in RBCs, vessels, interstitial tissue, and within cells

These glucose-protein complexes are called AGEs (advanced glycation end products)

64
Q

Why are AGEs problematic?

A

proteins, including albumin, LDLs, immunoglobulin, and complement get bound and trapped in the basement membrane

AGEs bidn to cell receptors of macrophages and glomerular mesangial cells, causing inflammation, cytokines, fibrosis

Can inactivate nitric oxide, leading to vasodilation

bound endothelial cells are procoagulant

65
Q

What percentage of individuals with DM develop kidney disease?

A

50%!

66
Q

Which tubule is particularly vulnerable to damage from hyperglycemia?

A

Proximal tubule (high level of aerobic metabolism and energy requirements, doesn’t tolerate hypoxia well)

67
Q

What is the first manifestation of diabetic kidney disease?

A

microalbuminuria (30-300 mg/day)

68
Q

Sometimes, as patient with DM related nephropathy gets worsening kidney disease, their insulin requirements go down.

Why?

A

The kidney isn’t metabolizing insulin

69
Q

Diabetic neuropathy targets which nerve fibers preferentially?

A

Sensory fibers, specifically Polymodal C and A delta

70
Q

Which is related to the severity of diabetes:

microvascular or macrovascular

A

microvascular

Macrovascular is not related to the severity of the diabetes, and may be present with very mild disease symptoms

71
Q

How many diabetics end up dying of cardiovascular disease?

A

68%

72
Q

Why are diabetics so prone to infection?

A
  1. Poor sense (decreased vision and sensation)
  2. glycosylated RBCs impede release of O2, causing hypoxia in most tissues
  3. pathogens proliferate rapidly thanks to all the glucose
  4. Decrease blood supply from capillary disfunction
  5. supressed immune response
  6. delayed wound healing d/t slower collagen synethies and decreased angiogenesis
73
Q

Hyperfunction of the adrenal cortex leads to _____ disease

Hypofunction of the adrenal cortex leads to _____ disease

A

Cushing Syndrome

Addison Disease

74
Q

Is cushing syndrome more common in men or women?

A

Women

75
Q

What’s the difference between

cushing syndrome

cushing disease

cushingoid syndrome

A

syndrome refers to the effects of excess endogenous cortisol

disease refers specifically to excess endogenous secretion of ACTH (corticotropin), which leads to excess cortisol or (more rarely) from an adrenal adenoma

side effect of prolonoged glucocorticoid drug therapy

76
Q

If someone has Cushing syndrome caused by excess ACTH, their ACTH levels will always have three characteristics regardless of the root cause:

A
  1. Non-diurnal or circadian secretion pattern
  2. No increase in ACTH in response to a stressor
  3. Depressed levels of CRH
77
Q

In patients with Cushing syndrome who do NOT have elevated levels of ACTH or CRH, the problem must be:

A

Excess cortisol secretion from a tumor in the adrenal cortex

78
Q

Patients with ACTH-independent Cushing’s often have an atrophied adrenal cortex. Why?

A

When the tumor produces massive amounts of cortisol, ACTH release is suppressed

This means the normal cells of the adrenal cortex aren’t being stimulated by ACTH at all, and they begin to atrophy

79
Q

What are the two reasons people gain weight with cushing syndrome?

A
  1. Truncal obesity (trunk, face, cervical area)
  2. Weight gain from sodium and water retention 2/2 the mineralocorticoid effect of cortisol at high levels
80
Q

Why do patients with elevated cortisol have hyperglycemia?

A

cortisol causes:

insulin resistance

gluconeogenesis

81
Q

Why does excess cortisol cause fatty deposits?

A

cortisol stimulates lipolysis by stimulating the production of lipases in adipocytes, which chomp the adipocyte into glycerol and fatty acids

glycerol is then used by the liver to make glycogen/glucose

BUT the fatty acids are left free to roam, and wind up depositing in weird places throughout the body

82
Q

What does the liver use to create glucose from non-carb products?

A

Amino Acids + glycerol = glucose

(proteins + lipids = glucose)

It can ALSO use lactic acid

83
Q

Why does excess cortisol cause high blood pressure and glycogenolysis?

A

It sensitizes the adrenergic receptors, making them more responsive to NE

in the blood vessels, this leads to vasoconstriction

in the liver, it leads to glycogenolysis

84
Q

Why do 20% of Cushing patients get renal stones?

A

increased osteoclasts activity results in bone resportion and hyperciurea

85
Q

What causes congenital adrenal hyperplasia?

A

deficiency of an enzyme that synthesizes cortisol results in low cortisol production (usually 21-hydroxylase)

ACTH increases, causing hyperplasia of the adrenal gland

86
Q

What causes Conn Syndrome?

A

Hypersecretion of aldosterone from the adrenal cortex

Usually caused by a unilateral benign adrenal adenoma

87
Q

Primary Hyperaldosterism has very different effects that secondary. Why?

A

Primary occurs in the absence of Angiotensin II, so it has effects that are out of balance with the perceived needs of the body:

Hypokalemia

insulin resistance

inflammation

LV remodeling

88
Q

What are some causes of secondary aldosteronism?

A

Anything that’s increasing Angiotensin II production:

hypovolemia

hypoperfusion

Bartter Syndrome

89
Q

What are the hallmarks of excess aldosterone?

A

hypertension

hypokalemia

hypervolemia

alkalosis

DOES NOT CAUSE EDEMA (pressure natriuresis - which worsens hypokalemia)

90
Q

Hypersecretion of estrogen causes:

Hypersecretion of androgens causes:

A

feminization

virilization

91
Q

Primary hypocortisolism is better known as:

A

Addison Disease

Need to “Add” Aldosterone

92
Q

What is the most common cause of Addison Disease?

A

autoimmune destruction of the adrenal cortex

93
Q

Addison Disease is characterized by: (3)

A

inadequate corticosteroid and mineralocorticoid synthesis

elevated serum ACTH

90 % loss of adrenocortical tissue

94
Q

Which enzyme is targeted in autoimmune destruction of the adrenal cortex?

A

21-Hydroxylase!

95
Q

People with Addison disease will have low levels of _____ AND ______

A

cortisol

aldosterone

96
Q

What happens in adrenal crisis?

A

Severe hypovolemia caused by Addison disease

Sparked by undiagnosed disease, acute withdrawal from steroids, or a concurrent infection/stressful event

97
Q

Patients with Addison disease exhibit ____ glucose levels and ____blood pressure

A

low

low

98
Q

What causes secondary hypocortisolism?

A

decreased ACTH 2/2 long term steroid therapy means adrenal glands atrophy and shrink

when steroid therapy is stopped, glands can’t produce enough cortisol on their own

99
Q

Secreting tumors of the adrenal medulla are rare. They include which two tumors?

A

pheochromocytomas

sympathetic paragongliomas

100
Q

Pheochromocytomas and sympathetic paragangliomas cause uncontrolled production of __________

A

Primarily norepinephrine

Really big ones will also secrete epinephrine

101
Q

Ingestion of what kinds of foods can spark a hypertensive crisis in a patient with an adrenal medulla mass?

A

Tyrosine-containing foods:

Aged cheese

red wine

beer

yogurt

AND caffeine

102
Q

What is usually the first sign of a pheochromocytoma?

A

hypertension that is unresponsive to drug therapy

103
Q

Why do patients with pheochromocytomas have glucose intolerance?

A

Catecholamines inhibit insulin release from the pancreas

Patho 2 (24 decks)

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