Brainscape's Knowledge GenomeTM

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


See full index

Endocrinology > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

Causes of Hypothyrodism

A

atomidine, kelp, lithium

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

Thyroid Hormone Effects

A
  • Fetal development (baby makes @ week 11)
  • Oxygen consumption & heat production
  • CV effects
  • Sympathetic effects
  • Pulmonary effects
  • GI effects
  • Skeletal effects
  • Lipid & Carbohydrates
  • Endocrine Effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Symptoms of Hypothyroidism

A
  • fatigue, weakness
  • dry skin
  • feeling cold
  • hair loss
  • memory
  • constipation
  • weight gain w/poor appetite
  • menorhagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Signs of Hypothyroidism

A
  • dry, coarse skin
  • puffy face, hands, feet
  • diffuse allopecia
  • bradycardia
  • peripheral edema
  • carpal tunnel syndrome
  • serous cavity effusions
  • delayed tendon reflex relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Symptoms of Hyperthyroidism

A
  • fatigue/weakness
  • hyperactivity, irritability, dysphoria
  • heat intolerance/sweating
  • palpitations
  • weight loss with increased appetite
  • diarrhea
  • oligomenorrhea, loss of libido
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Signs of Hyperthyroidism

A
  • tachycardia, atrial fibrillation in elderly
  • tremor
  • goiter
  • warm, moist skin
  • muscle weakness, proximal myopathy
  • Lid retraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lab Assessment of TF

A
  • TSH
  • T4 - total and free
  • T3 - total and free
  • T3 index
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hyperthyroidism

A
  • TSH secretion pituitary adenoma

- isolated pituitary resistance to thyroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypothyroidism

A

-Central hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Euthyroid

A
  • systemic illness
  • generalized resistance
  • assay interference
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Etiology of Hyperthyroidism

A 
-Endogenous
   Graves disease
   Toxic multinodular goiter
   Toxic adenoma
   Activation mutation of TSH receptor
   Activation mutation of Gs(alpha)
   Struma ovarii
   Thyroiditis
   Secondary hyperthyroidism
-Exogenous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Etiology of Primary Hypothyroidism

A
  • Thyroiditis
  • RIA tx for Graves Disease
  • Thyroidectomy
  • Excessive Iodine Intake
  • Iodine Deficiency
  • Inborne errors of TH synthesis
  • Drugs (Lithium, Amiodarone, Interferon-alpha)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Etiology of Secondary/Tertiary Hypothyroidism

A
  • destruction of pituitary gland
  • hypothalamic dysfunction
  • peripheral resistance to thyroid hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Classification of Thyroiditis

A
  • acute
  • subacute
  • silent
  • Riedel’s thyroiditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Thyroid Enlargement

A
  • diffuse nontoxic (simple) goiter
  • nontoxic multinodular goiter
  • toxic multinodular goiter
  • hyperfunctioning solitary nodule
  • thyroid neoplasm/cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What hormones are secreted by the neurohypophysis (posterior pituitary)?

A

Vasopressin & Oxytocin
similar to each other - nonapeptides that differ with 2 amino acids
-ring structure with disulfide linkage
SITE: in magnocellular neurons of supraoptic and paraventricular nuclei of hypothalamus, biosynthesized in diff. cell bodies by macromolecular precursors that are cleaved to yeild active hormone, linking protein (neurophysin) & other peptides
-stored in vesicles at the end of neurosecretory axons in posterior pit. and secreted by Ca-dep. exocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Human Vasopressin

A

called arginine vasopressin (AVP)
also called antidiuretic hormone (ADH)
-nonapeptides similar to oxytocin with only 2 amino acid difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Actions of Vasopressin

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

Vasopressin Receptor Types

A

V(A1): CV -cause vasoconstriction, in myocardium causes increase in afterload & hypertrophy
V(1B): ant. pit. & median eminence mediate ACTH release
V(2): renal effects, conserves water and concentrates the urine by enhancing the hydro-osmotic flow of water from the luminal fluid through the cells of the collecting tubule of kidney to medullary interstitium

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

Normal Vasopressin Levels

A

-blood conc. fluctuates
max: late night/early morning
min: early afternoon
2.5-8ng/l
inactivation occurs in liver & kidney
7-10% excreted in urine as active hormone

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

Stimuli that lead to release of vasopressin?

A

1) increase in plasma osmolarity
2) decrease in plasma volume
3) activation of carotid/aortic baroreceptors in response to hypotension
4) cholinergic/beta-adrenergic stimuli (+)
atropine & alpha-adrenergic stimulation inhibit (-)
5) aging increases release (60+)
6) drugs can (+), nicotine (+), ethanol (-)
7) H2O deprivation (+), H2O administration (-)
osmotic factors normally control, but override by blood volume if >10% change
8) cortisol (-)

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

Water Porin Channel regulated by Vasopressin?

A

AQP2 in the kidney

-conditions associated with H2O retention like CHF, pregnancy, SIADH are accompanied by increased expression of AQP2

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

Central Diabetes Insipidus

A

“Neurogenic DI”

  • failure to conc. urine as a result of decreased secretion of osmoregulated AVP
  • uncommon (1 in 25,000)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Central Diabetes Insipidus

Signs/Symptoms

A

-polyuria-day and night
-polydipsia (want ice-cold water)
-thirst
kids (enuresis)
-nocturia: chronic tiredness, poor school/work, malaise

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

Central Diabetes Insipidus

Etiology

A

-familial or acquired
-inherited AD or Recessive
Majority are acquired
(idiopathic (30% AVP abs), brain tumors, head trauma, granulomas of hypo-pit. area, CNS infection, Cerebral vascular disorders)

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

Pathophysiology of Polyuria

A

1) insufficient osmoregulated AVP (neruogenic DI)
2) complete/partial renal resistance to antiduretic action of AVP (nephrogenic DI)
3) habitual fluid drinking or primary polydipsia:
psychiatric illness
- abnormal thirst mechanism of idiopathic/specific etiology

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

Diagnosis of Polyuria

A
  • endocrine investigations

- urine volume > 2.5L in 24hrs

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

Neurogenic Polyuria

A

water deprivation osmolality increase with dilute urine, give AVP and renal tubules will respond and urine osmolality increase to over 750 mOsm/kg
-low AVP that doesn’t increases with hypertonic saline solution

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

Nephrogenic Polyuria

A
  • plasma osmolality in high/normal range
  • low urine osmolarity
  • fail to respond to water deprivation, urine osmolality remains low and serum osmolality gets very high
  • does NOT respond to AVP
  • increase AVP with hypertonic saline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Primary Polydypsia

A

-low random plasma osmolality, low urine osmolality
-respond to water deprivation-increase urine osmolality (no defect in AVP secretion/action
-respond to AVP and increase urine osmolality
(if after lots of H2O though, its already saturated)
-increase AVP with hypertonic saline infusion

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

SIADH

A

“syndrom of inappropriate secretion of ADH”

  • plasma vasopressin conc. inappropriately high for plasma osmolality
  • with normal water intake, water retention, leading to hyponatremia and hypo-osmolality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Causes of SIADH

A

1) malignant tumors with autonomous AVP release (carcinoma of lung)
2) nonmalignant pulmonary diseases (TB)
3) Central Nervous System (meningitis)
4) Drugs (narcotics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Malignant tumors with AVP

A
  • stored and autonomously released from tumor tissue in amounts that are determined largely by the tumor mass and not by known stimuli
  • small cell/oat cell carcinoma of lung 80%*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Nonmalignant Pulmonary diseases with AVP

A
  • acquires the capacity to synthesize and release AVP autonomously or reduces left atrial filling with stimulates central AVP release
  • hyponatremia is common feature of pulmonary TB and pneumonia
35
Q

Release of AVP from patients neurohypophysis?

A

-due to neighboring inflammatory, neoplastic, or vascular lesions or drugs and independently of normal stimuli

36
Q

Clinical/Laboratory features of SIADH?

A

-weight gain
-weakness
-lethargy/mental confusion
-convulsions and coma
Lab: low serum BUN, creatinine, uric acid, albumin
Na < 130mEq/L, osm < 270, urine is hypertonic
urine Na > 20

37
Q

Treatment of SIADH?

A

1) treat underlying cause/remove drug
2) H2O restriction to no more than 1000mL/24 hrs
3) Drugs that block AVP on distal and convoluted tubules of the kidney, Li has numerous adverse effects, demeclocycline must be used with caution in patients with hepatic dysfunction
4) Very careful infusion of hypertonic saline
5) “Vaptans” 3 AVP receptor subtypes are members of rhodopsin-like G-protein-coupled receptor family
- non-peptide AVP V2 antagonists have been developed to treat hyopnatremia

38
Q

Stimuli for Oxytocin Release

A
  • mechanical distention of the reproductive tract (vagina)

- suckling of the nipples

39
Q

Actions of Oxytocin

A
  • stimulation of uterine contractions at partutition

- augmentation of intramammary pressure during suckling

40
Q

Amount of Oxytocin

A
  • pharm doses like in pregnancy (labor) can alter metabolism of water by kidney (1 unit of oxytocin has 0.01 units of ADA) due to biological similarity to ADH
  • severe H2O intoxication in women infused with oxytocin at high rates & given hypotonic fluids
41
Q

Other roles of Oxytocin/location of secreting cells

A
  • Magnocellular neurons of hypothalamic paraventricular and supraoptic nuclei, smaller cells scattered around brain secrete also
  • learning, anxiety, feeding, pain perception
  • modulate social memory, attachment, sexual/material behavior, aggression, human bonding, trust
42
Q

Adrenohypophysiotropic Neurones

A
  • synthesize and secrete peptides or bioamine hormones directly into fenestrated capillaries specialized to receive hormone granules at azonal-capillary terminations in the median eminence (tuber cinereum)
  • transported down pit. stalk via a network of fine vessels called the hypophyseal portal venous system, which terminates in capillaries surrounding the anterior pituitary
43
Q

GnRH Stimulates?

A
  • FSH

- LH

44
Q

GHRH Stimulaties?

A

-GH

45
Q

TRH Stimulates?

A
  • TSH

- Prolactin

46
Q

VIP PHI-27 Stimulates?

A

-Prolactin

47
Q

CRH & ADH

A

-ACTH
beta-lipotrophin
beta-endorphin

48
Q

Somatostatin Inhibits?

A
  • GH

- TSH

49
Q

Dopamine Inhibits?

A
  • TSH

- Prolactin

50
Q

Neurohypophysiotrophic Neurons

A
  • magnocellular (large, long) synthesizing antidiuretic hormone (ADH) and oxytocin
  • stored in and secreted from post. pit. directly into systemic blood
51
Q

Negative Feedback

A

-increase in level of target gland hormone suppresses the secretion of its corresponding pituitary trophic hormone, or the appropriate hypothalamic releasing hormone

52
Q

Positive Feedback

A

-an increase in the level of the target gland hormone produces an increased secretion of the corresponding trophic or releasing hormone

53
Q

Long-loop Feedback

A

-target gland hormone regulates secretion at hypothalamic and/or pituitary

54
Q

Short-loop Feedback

A

-pituitary gland hormone modulates one or more hypothalamic-releasing hormones

55
Q

Ultra-short Feedback

A

-a hypothalamic hormone influences the secretion of its own hormone secreting neurone (autoaxonal inhibition) or an adjacent neurone (para-axonal inhibition)

56
Q

Neurosecretion

A

Pulsatility: occures ~every 20min, CRH, ACTH, cortisol, GnRH, LH, FSH, beta-estradiol

Diurnal rhythms: (circadian) time-dependent variation in circulating hormone levels in 24hr period, ACTH peak at 6-8am decrease during day

Sleep-related hormone secretion: GH during day in slow pusatile bursts, 1-2 hr after sleep starts (stage 3-4) get burst of 70%, most in childern
-prolactin also in sleep

57
Q

Hypopituitarism

A

-partial or complete loss of secretion of one (monotrophic) or more (polytropic) pituitary hormones with clinical manifestations of pituitary failure

58
Q

Monotropic Hypopituitarism

A
  • isolated GH deficiency

- isolated LH/FSH deficiency; isolated ACTH deficiency (rare) isolated TSH deficiency (rare)

59
Q

Polytropic Hypopituitarism

A

GH, PRL, LH/FSH, TSH and ACTH deficiency in various combinations

60
Q

Panhypopituitarism

A

anterior and posterior pituitary failure

61
Q

How much destruction of pituitary affects?

A

50% no consequences
65-75% moderate effects
90% severe hypopituitarism
compression lesions: expanding pit. tumors gonadotrophic & GH failure, then PRL, TSH, ACTH deficiencies

62
Q

Causes of Hypopituitarism

A

1) pituitary lesions, which lead to primary hypopituitarism

2) hypothalamic lesions, which lead to secondary hypopituitarism

63
Q

Mechanisms of Hypopituitarism

A

1) Tumors
2) Vascular Infarction
3) Inflammatory Lesions
4) Infiltration
5) Head or post-surgical Trauma
6) “Idiopathic” Hypopituitarism
7) Autoimmune Hypophysitis
8) Empty Sella

64
Q

Hypothalamic Disorders

A
  • various diseases or conditions that involve the hypothalamus may affect the secretion of the hypothalamic hormones which in turn influence the secretion of corresponding pituitary hormones
  • include diminution in the secretion of vasopressin with resulting diabetes insipidus
65
Q

Mechanisms of Hypothalamic Disorders

A
  • infiltrative disorders
  • mass lesions
  • radiation
  • infection
  • trauma
66
Q

TSH Deficiency

A

-low T4, low T3
-low/normal TSH
Hypothyroidism: weight gain, no energy, cold intolerance, sluggishness, dry cool skin, delayed relaxation of reflexes

67
Q

ACTH Deficiency

A

-low cortisol
-low androgens
Hypoadrenalism: hypotension, anorexia, weight loss, aches, pains, loss or axillary hair in wome

68
Q

LH/FSH Deficiency

A

-low testosterone
-low estradiol/progesterone (female)
Hypogonadism:
Men:Impotence, infertilit
Women: amenorrhea, infertility

69
Q

GH Deficiency

A 
-low somatomedin-C (IgF1)
Growth Failure: short stature (children)
 insulin sensitivity (adults), premature aging
70
Q

PRL Deficiency

A 
-low PRL
Failed lactation (adult): alactia
71
Q

Static Test

A

-measure basal (unstimulated) levels

72
Q

Dynadmic Test

A

-measure stimulated levels following maximal but safe doses of various stimuli

73
Q

Acromegaly: Elevated GH

A

-loss of nocturnal stage III sleep rise, elevated IgF1

74
Q

Acromegaly: Elevated IFG-I (somatomedin-C)

A

-increased growth of cartilaginous bones
-increased soft tissue mass and sweat gland hypertrophy
Prognathism, splaying out of teeth, large nose, hands & feet, large nasal sinuses
-thickened skin & subcutaneous tissue, skin tags, excessive sweating

75
Q

Acromegaly: Elevated GH and/or IGF-I

A

-visceral enlargement
-insulin resistance
Large liver, spleen, kidney
Glucose intolerance or diabetes

76
Q

Acromegaly: Elevated GH and PRL (mixed tumors)

A

-Galactorrhea & hypogonadism with acromegaly

Infertility, with acromegaly

77
Q

Elevated PRL in Adult Men

A

-decreased GnRH
-decreased LH/FSH
-decreased testosterone
decreased libido
impotence
infertility
HYPOGONADISM

78
Q

Elevated PRL in Adult Women

A

-decreased GnRH
-decreased LH/FSH
-decrease estradiol & progesterone
anovulation
amenorrhea
galactorrhea
infertility
osteopenia
-Increased adrenal androgen secretion = hirsutism
HYPOGONADISM

79
Q

Cushing’s: Elevated ACTH

A

-bilateral adrenal hyperplasia with increased plasma cortisol and adrenal androgen
-loss of diurnal rhythm of ACTH & cortisol
-increased urinary cortisol
increased skin pigmentation due to elevated ACTH

80
Q

Cushing’s: Elevated Cortisol

A

-salt retention insulin resistance, increase fat deposits
-decreased skin collagen
-proximal myopathy
-cerebral effects
HTN, hyperglycemia, diabetes mellitus, obesity (central, buffalo hump, supraclavicular fat pad)
easy bruisability, striae, girdle muscle weakness, depression, emotional lability, psychosis

81
Q

Cushing’s: Elevated Adrenal Androgen

A
  • hair growth = hirsutism
  • decreased LH/FSH secretion = oligomenorrhea
  • increased sebum production = acne, oily skin
  • decreased libido = impotence
82
Q

Gonadotroph Adenomas

A
  • most common pituitary macroadenoma
  • difficult to recognize because nonfunctioning
  • usually recognized when large enough to produce neurological symptoms: visual impairment, but headache, diplopia, CSF rhinorrhea, pituitary apoplexy caused by sudden hemorrhage into the adenoma, and others may occur
83
Q

TSH-secreting adenomas

A

-rare NOT usual cause of hyperthyroidism, but most cause thyrotoxicosis
-large, 1/3 associated with acromegaly or hyperprolactinemia
-no TSH response to TRH nor TSH suppression to exogenous thyroid hormone
-suppressed by glucocorticoids /somatostatin analog
-85% have elevated alpha subunits in serum
male=female

Endocrinology (15 decks)

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