Brainscape's Knowledge GenomeTM

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


See full index

Pathophysiology > 19. Endocrine Alterations > Flashcards

19. Endocrine Alterations Flashcards

1
Q

List the 7 hormones released from the anterior pituitary and their target tissues

A
  • Prolactin (mammary gland) - ACTH (adrenal cortex) - GH (bone/muscle/tissues) - TSH (thyroid gland) - LH + FSH (ovaries and testes) - MSH (melanin in skin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the function of the posterior pituitary?

A

stores ADH and oxytocin produced by the hypothalamus; DOES NOT PRODUCE THEM!

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

What are the 3 direct targets of the hypothalamus and through what?

A
  • anterior pituitary: through releasing hormones (RH) and inhibiting hormones (IH) - kidneys and uterus/breast: through ADH and oxytocin - adrenal medulla: sympathetic innervation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do pancreatic B cells secrete?

A

insulin and C peptide (aka Amylin)

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

What do pancreatic A cells secrete?

A

glucagon

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

What do pancreatic D cells secrete?

A

somatostatin

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

What do pancreatic F cells secrete?

A

pancreatic polypeptide

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

What causes pituitary dwarfism? What do these people look like?

A
  • hyposecretion of growth hormone - normal body proportion but rarely taller than 4ft
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes acromegaly? Most common cause?

A
  • caused by continuous exposure to high levels of GH and insulin-like growth factor 1 (IGF-1) - almost always caused by GH-secreting pituitary adenoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acromegaly vs gigantism

A
  • acromegaly: occurs in adults (after growth plates have close) - gigantism: occurs in childhood (before growth plates close)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

condition that results from any cause of increased TH levels

A

thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

form of thyrotoxicosis in which excess amounts of TH are secreted from the thyroid gland

A

hyperthyroidism

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

clinical manifestations of hyperthyroidism

A
  • thin hair - tachycardia - weight loss (elevated metabolism) - exophthalmos (protruding eyes) - hyperreflexia - enlarged thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

over secretion of T3/T4 due to abnormal antibodies (TSIs) that stimulate TSH receptors (type II hypersensitivity)

A

Grave’s disease

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

What causes goiters?

A

thyroid enlargement due to iodine deficiency - follicles make thyroglobulin but cannot make TH

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

subcutaneous swelling on the anterior portions of the legs and indurated and erythematous skin; seen w/ high levels of TSI

A

pretibial myxedema (Grave’s dermopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  • occurs when there are several hyper-functioning nodules leading to hyperthyroidism - what is it called when only 1 nodule is hyper-functioning?
A
  • toxic multinodular goiter - toxic adenoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

dangerous worsening of thyrotoxic state in which death can occur within 48 hours without treatment; sxs caused by increased action of T4 and T3 exceeding metabolic demands

A

thyrotoxic crisis (thyroid storm)

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

Sxs of thyrotoxic crisis

A
  • hyperthermia - tachycardia - high output heart failure - agitation/delirium - N/V/D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Grave’s diseases is a _____ hyperthyroidism and a TSH-secreting pituitary adenoma is a ____ hyperthyroidism

A
  • primary - secondary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

congenital iodine deficiency/hypothyroidism

A

cretinism

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

clinical manifestation of cretinism

A
  • difficulty eating - protruding tongue - hypotonia - lethargy - bradycardia - cognitive disability varies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

deficient production of TH by the thyroid gland

A

hypothyroidism

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

most common form of primary hypothyroidism; gradual inflammatory destruction of thyroid tissue by infiltration of auto reactive T lymphocytes and circulating thyroid antibodies

A

autoimmune thyroiditis (Hashimoto’s thyroiditis)

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

rare nonbacterial inflammation of the thyroid gland often preceded by a viral infection; associated w/ transient hypothyroidism

A

subacute thyroiditis (de Quervain thyroiditis)

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

clinical manifestations of hypothyroidism

A
  • loss of hair - bradycardia - decreased metabolism - lethargy - cold intolerance - muscle weakness - LE edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

characteristic sign of severe or long-standing hypothyroidism; will see non pitting, boggy edema (around eyes, hands, feet, and supraclavicular fossa), slurred speech, and hoarseness

A

myxedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

clinical manifestation of myxedema coma (medical emergency)

A
  • hypothermia w/o shivering - hypoventilation - hypotension - hypoglycemia - lactic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

most common endocrine malignancy

A

thyroid carcinoma

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

high levels of ADH in the absence of normal physiologic stimuli for release

A

syndrome of inappropriate ADH secretion (SIADH)

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

How does SIADH affect the following: - urine output - urine osmolality - serum Na - serum osmolality

A
  • urine output: low - urine osmolality: high - serum Na: low (hyponatremia) - serum osmolality: low (hypoosmolar)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

symptoms of SIADH

A
  • water retention - low urine output - N/V - mental changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the overall function of ADH?

A

increases BP and blood volume, decreases osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

failure of hypothalamus to produce ADH or release it from posterior pituitary; decrease in ADH plasma levels

A

neurogenic/central diabetes insipidus (DI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

kidneys unable to respond to ADH; increase plasma ADH

A

nephrogenic diabetes insipidus (DI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does DI affect the following: - urine output - urine osmolality - serum Na - serum osmolality

A
  • urine output: high - urine osmolality: low - serum Na: high (hypernatremia) - serum osmolality: high (hyperosmolar)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

symptoms of DI

A
  • polyuria - thirst - high urine output - signs of dehydration
38
Q

treatment of SIADH

A
  • fluid restriction - treat the cause
39
Q

treatment of DI

A
  • give desmopressin (synthetic analog of ADH) -> central - treat the cause -> nephrogenic
40
Q

benign, slow-growing tumors that arise from cells in the anterior pituitary

A

pituitary adenoma

41
Q

3 most common types of pituitary adenoma

A
  • Prolactinoma (60%) - Acromegaly/giantism (20%) - Cushing’s disease (10%)
42
Q

characterized by greater than normal secretion of PTH and hypercalcemia

A

hyperparathyroidism

43
Q

characterized by inappropriate excess secretion of PTH by one or more of the parathyroid glands

A

primary hyperparathyroidism

44
Q

compensatory response of parathyroid glands to chronic hypocalcemia -> can be associated w/ decreased renal activation of vitamin D (renal failure)

A

secondary hyperparathyroidism

45
Q

How does hyperparathyroidism affect Ca and Pi

A
  • increased Ca levels (hypercalcemia) -> increases bone resorption to release Ca and GI reabsorption - decreased Pi levels (hypophosphatemia) -> PTH causes Pi to be excreted in urine
46
Q

clinical manifestations of primary hyperparathyroidism

A
  • fatigue - headache - depression - anorexia - N/V - pathologic fractures
47
Q

abnormally low PTH levels most commonly caused by damage to parathyroid glands during thyroid surgery

A

hypoparathyroidism

48
Q

How does hypoparathyroidism affect Ca and Pi

A
  • decreased Ca levels (hypocalcemia) - increased Pi levels (hyperphosphatemia)
49
Q

clinical manifestations of hypoparathyroidism

A
  • symptoms of hypocalcemia (ex. tetany and muscle spasms) - dry skin - loss of body and scalp hair - hypoplasia of developing teeth - bone deformities
50
Q

refers to clinical manifestations resulting from chronic exposure to excess cortisol regardless of cause

A

Cushing syndrome

51
Q

hypersecretion of ACTH

A

Cushing disease

52
Q

clinical manifestations of Cushing’s syndrome

A
  • fat deposition on neck/back (buffalo hump) - fat deposition on the face (moon face) - ABD fat deposition - bruising (breakdown of collagen) - stretch marks - muscle weakness/wasting - osteoporosis - adrenal hyperplasia
53
Q

How would Cushing disease affect the following values: - K - Na - glucose

A
  • K: hypokalemia (aldosterone -> K excretion) - Na: hypernatremia (aldosterone -> Na reabsorption) - glucose: hyperglycemia (high cortisol)
54
Q

primary adrenal insufficiency (hyposecretion of all adrenal steroids) usually due to autoimmune restriction of adrenal gland

A

Addison’s disease

55
Q

How would Addison’s disease affect the following values: - K - Na - glucose

A
  • K: hyperkalemia (no aldosterone for K excretion) - Na: hyponatremia (no aldosterone for Na reabsorption) - glucose: hypoglycemia (low cortisol)
56
Q

clinical manifestations of Addison’s diseases

A
  • weakness/fatigue - skin hyperpigmentation (due to high MSH associated w/ high ACTH) - hypotension - tachycardia - N/V/D - adrenal atrophy
57
Q

hyper-secretion of aldosterone due to adrenal neoplasm

A

primary hyperaldosteronism (Conn syndrome)

58
Q

tumor of chromaffin tissue -> produces excess catecholamines

A

pheochromocytoma

59
Q

Symptoms of pheochromocytoma

A
  • persistant HTN - headache - pallor - diaphoresis - tachycardia/palpitations - anxiety
60
Q

permanent attachment of glucose to hemoglobin and reflects average plasma glucose exposure of life of RBC

A

glycosylated hemoglobin (HbA1c)

61
Q

lab value diagnosis criteria for DM

A
  • HbA1c > 6.5% - fasting plasma glucose (FPG) > 126 mg/dl (fasting = at least 8 hours) - 2 hour plasma glucose > 200 mg/dl during oral glucose tolerance test (OGTT) - symptoms of hyperglycemia w/ random plasma glucose > 200 mg/dl
62
Q

beta cell destruction -> leads to absolute insulin deficiency

A

type 1 DM (IDDM)

63
Q

Describe pathophysiology of IDDM

A
  • autoantigens form on B-cells and circulate in bloodstream/lymphatics - activation of cellular immunity (T cells) and humoral immunity (autoantibodies) towards B-cells - destruction of B-cells with decreased insulin secretion
64
Q

How does a decrease in insulin affect glucagon levels?

A

causes increase in glucagon (produced by alpha cells of pancreas)

65
Q

clinical manifestations of IDDM

A
  • polydipsia (water attracted to glucose -> intracellular dehydration) - polyuria (hyperglycemia = osmotic diuretic) - polyphagia (depletion of cellular stores due to lack of glucose -> starvation) - weight loss - fatigue - visual changes - paresthesias
66
Q

What is one of the most important contributors to insulin resistance and NIDDM

A

obesity

67
Q

4 mechanisms that link obesity to insulin resistance

A
  • inflammation changes adipokine levels - elevated levels of serum FFA and intracellular deposit of triglycerides (interfere w/ insulin signaling) - inflammatory cytokines released from adipocytes are cytotoxic to B-cells - obesity is correlated w/ hyperinsulenima and decreased insulin receptor density
68
Q

combination of insulin resistance and decreased beta cell mass and function

A

type 2 DM (NIDDM)

69
Q

clinical manifestations of NIDDM

A
  • some classic sxs (polyuria/polydipsia) - fatigue - pruritus - recurrent infections - visual changes - neuropathy - individual is usually overweight w/ dyslipidemia and HTN
70
Q

low blood glucose during the night that may lead to rise in morning blood glucose; tx is a nighttime snack to prevent hypoglycemia

A

Somogyi effect

71
Q

early morning rise in blood glucose level related to release of GH, cortisol, and catecholamines w/o preceding hypoglycemia; tx is insulin to counter hyperglycemia

A

dawn phenomenon

72
Q

symptoms of hypoglycemia

A
  • pallor - tremor - tachycardia/palpitations - diaphoresis - headache - irritability/anxiety - confusion - seizures - coma
73
Q

serious complication related to deficiency of insulin and increase in levels of insulin couter-regulatory hormones (catecholamines, GH, cortisol, and glucagon)

A

diabetic ketoacidosis (DKA)

74
Q

3 main characteristics of DKA

A
  • hyperglycemia - acidosis - ketonuria
75
Q

Why is DKA more common in IDDM?

A

insulin is more deficient

76
Q

Pathophysiology of DKA

A
  • w/ insulin deficiency -> lipolysis is enhanced (increased fatty acid delivery to liver) - increased glyconeogenesis (contribute to hyperglycemia and production of ketone bodies) - increased ketones -> decreased pH -> metabolic acidosis
77
Q

clinical manifestations of DKA

A
  • Kussmaul respirations - fruity/acetone odor in breath - CNS depression - ketonuria - anorexia - N/V and ABD pain - postural dizziness
78
Q

more common complication of NIDDM that differs from DKA w/ higher degree of fluid deficiency rather than insulin deficiency

A

hyperosmolar hyperglycemic nonketoic syndrome (HHNKS)

79
Q

In which disease are glucose levels higher: DKA or HHNKS?

A

HHNKS -> due to volume depletion

80
Q

clinical manifestations of HHNKS

A
  • severe dehydration (from polyuria) - loss of electrolytes (ex. potassium) - neurologic changes (stupor, coma, seizures) - hypotension/hypoperfusion/tachycardia - N/V and ABD pain
81
Q

List 7 chronic complications of DM

A
  • retinopathy - nephropathy - neuropathy - infection - CAD - stroke - PVD
82
Q

results from relative hypoxemia, damage to retinal blood vessels, RBC aggregation, and HTN

A

diabetic retinopathy

83
Q

glomeruli are injured by hyperglycemia w/ high renal blood flow (hyper filtration) and intraglomerular HTN

A

diabetic nephropathy

84
Q

most common complication of DM; hyperglycemia leads to ischemia and demyelination contributing to neural changes and delayed conduction

A

diabetic neuropathy

85
Q

clinical manifestation of diabetic neuropathy

A
  • glove and stocking loss of sensation - loss of motor nerve function w/ clawed toes and small muscle wasting in hands - Charcot joints (joint and ligament degeneration; mainly in feet)
86
Q

How does diabetic neuropathy lead to amputation?

A
  • decrease in sensation -> painless trauma -> ulceration -> infection - muscle atrophy -> changes in gait -> new pressure points -> ulceration -> infection - autonomic neuropathy -> decreased perspiration -> dry skin/cracks/fissures -> infection - All lead to soft tissue infection and osteomyelitis
87
Q

Other than diabetic neuropathy, what else leads to amputation for diabetics?

A

angiopathy of both large and small vessels (vessel occlusion -> ischemia -> gangrene)

88
Q

5 main reasons diabetics have increased risk for infection throughout the body

A
  • impaired senses (neuropathy and retinopathy) - hypoxia (glycosylated Hgb impaired O2 delivery to tissues) - pathogens (some proliferate rapidly due to high glucose levels) - blood supply (vascular changes and reduced supply of WBCs) - suppressed immune response (impaired innate and adaptive immune system)
89
Q

Goal of treatment for DM

A

prevent complications by regulating glucose - diet - exercise - medications

90
Q

Metabolic acidosis (ex. DKA) will do what to serum potassium levels?

A

increase (hyperkalemia) -> H+ replaces K in the cells

Pathophysiology (20 decks)

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