endocrine disorders Flashcards
1
Q
endocrine system functions
A
- contributes to processes involved in maintaining physiological equilibrium (homeostasis)
- includes all tissues or glands that secrete hormones into the blood
- hormones bond to specific receptors that allows the hormone to exert its effect
- > delivered to many tissues, but will ONLY affect those with the appropriate receptor
- > nervous system: neutrotransmitters, neurohormone
- > endocrine sysytem: hormones
- secretion of most hormones is regulated by a negative feedback system
2
Q
negative feedback
A
- primary mechanism through which the endocrine system maintains homeostasis
- secretion of specific hormones are turned “on” or “off” by specific physiological changes - like thermostat
- ex: plasma glucose levels and the insulin/glucagon response - eating raises blood glucose, pancreas releases insulin
3
Q
why is the hypothalamus so important
A
- “master gland”
- major link between nervous and endocrine system
4
Q
pituitary attached to hypothalamus by [ ]
A
- by infundibulum
- pituitary has 2 parts
1. posterior pituitary: storage site for 2 hormones
2. anterior pituitary: synthesis and release
5
Q
what does the hypothalamus do
A
- synthesizes and secretes “regulatory” hormones
* releasing hormones: stimulate release of anterior pituitary hormones
* release inhibitory hormones: inhibit release of anterior pituitary hormones
* “directs” pituitary gland (hypophysis) - synthesizes 2 hormones that are stored in posterior pituitary
* oxytocin - the love hormone
* vasopression (also called antidiuretic hormone (ADH))
6
Q
releasing hormones
A
- regulatory hormone from hypothalamus
- stimulate release of anterior pituitary hormones
7
Q
release inhibitory hormones
A
- regulatory from hypothalamus
- inhibit release of anterior pituitary hormones
8
Q
hormones stored in posterior pituitary
A
- oxytocin and vasopression/ADH
- synthesized by hypothalamus
9
Q
hypothalamus and anterior pituitary
A
- hypothalamus produces releasing and inhibiting hormones
- hypophyseal portal system: connect hypothalamus to pituitary
10
Q
secretory hypothalamus
A
- hypothalamus synthesizes and secretes a variety of regulatory hormones
- hypothalamic releasing/inhibitory factors act upon anterior pituitary
- direct relase of anterior pituitary hormones
- hypothalamus can release GHRH (growth hormone releasing hormone) and SS (somatostatin/GH inhibitory hormone)
11
Q
hypophyseal portal system
A
12
Q
hypothalamic releasing hormones and effects on pituitary
A
- corticotropin releasing hormone (CRH): stimluates adrenocorticotropic hormone (ACTH) secretion
- thyrotropin releasing hormone (TRH): stimulates thyroid stimulating hormone (TSH) and prolactin
- growth hormone releasing hormone (GHRH): stimualtes growth hormone (GH) secretion
- somatostatin (growth hormone-inhibiting hormone [GHIH]): inhibits GH secretion
- gonadotropin releasing hormone (GnRH/LHRH): stimulates LH and FSH secretion
- prolactin releasing hormone (PRH): stimulates prolactin secretion
- prolactin inhibiting hormone (dopamine): inhibits prolactin secretion
13
Q
pituitary disorders
A
- pituitary tumors account for ~10-15% of intracranial tumors
- majority are an adenoma - a benign tumor
- pituitary close proximity to optic nerve: changes in vision, HA, nausea
14
Q
what happens in pituitary disorders
A
- result in too much or too little hormone release
- hyperpituitarism
- > acromegaly/gigantism (increased growth hormone)
- > Cushing’s disease (increased cortisol) - syndrome in adrenals
- hypopituitarism
- > diabetes insipidus (decreased vasopression [ADH]): like DM but no change in normal blood glucose
- common symptoms
- HA, vision changes, lethargy/fatigue, nausea and vomiting, nasal drainage, behavioral changes (hostility, depression), changes in sense of smell
15
Q
growth hormone (GH) disorders
A
- gigantism: excessive secretion of GH in children, epiphyseal plate not yet closed
- acromegaly: excessive secretion of GH in adults, most often in 4th decade, slow but continuous progression (andre the giant)
16
Q
posterior pituitary (neurohypophysis)
A
- stores releases 2 hormones
1. ADH (vasopressin): anti-diruetic hormone - increases BP
2. oxytocin
17
Q
vasopressin (anti-diretic hormone [ADH])
A
- regulates blood volume/pressure and salt concentration (plasma osmolarity)
- cells of supraoptic and paraventricular nuclei are osmoreceptors - how much water
- posterior pituitary secretes vasopressin (ADH) in response to:
- > reduced blood volume (baroreceptors sense low BP)
- > increased plasma osmotic pressure (osmoreceptors in the hypothalamus sense increased solute in blood)
18
Q
does ADH increase or decrease during happy hour
A
- goes down - pee a lot
19
Q
diabetes insipidus (DI)
A
- loss of ADH production
- no issue with glucose metabolism
- characterized by excretion of large volume of urine (polyuria - low BP) and excessive thirst (polydipsia) and increased appetite (polyphagia)
- 2 causes
1. posterior pituitary doesn’t secrete ADH - central/neurogenic DI
2. insensitivity of kidney to ADH - nephrogenic DI
20
Q
diagnosis and symptoms of diabetes insipidus (DI)
A
- diagnosis
- NO hyperglycemia
- dilute urine
- blood test: hypernatremia and increased plasma osmolality
- signs and symptoms
- 3 Ps: polydipsia, polyuria, polyphagia
- hypovolemia and dehydration: dizziness, hypotension, seizures
- muscle weakness/fatigue
21
Q
adrenal disorders
A
- hyperfunction
- Cushing’s disease/syndrome
- hyperaldosteronsim (Conn’s syndrome)
- pheochromocytoma
- hypofunction
- hypoaldosteronism/hypocortisolism (Addison’s disease)
22
Q
cortisol
A
- normally, release of cortisol is controlled by the hypothalamus:
- hypothalamus secretes corticotropin-releasing hormone (CRH)
- CRH triggers the anterior pituitary to secrete adrenocorticotropic hormone (ACTH) into the vascular system
- ACTH is carried in the blood to the adrenal cortex stimulating the synthesis of cortisol
- pituitary tumors: hyper ACTH – hyper-cortisol (hyperglycemia, osteoporosis, muscle fatigue)
23
Q
normally, as cortisol synthesis increases, what happens to CRH production
A
goes down
24
Q
common functions of cortisol
A
- counter-regulatory to insulin: promotes hyperglycemia
- decreases bone formation (decreased osteoblast function) and decreases intestinal Ca++ absorption
- acts as a diuretic
- influences immune function: inhibits production/release of inflammatory mediators
25
Q
osteoblasts vs osteoclasts
A
- osteoblasts build bone
- osteoclasts eats up bone
26
Q
cushing’s disease/syndrome
A
- hypersecretion of cortisol
- cushing’s disease - pituitary cushing’s (CNS)
- cushing’s syndrome - adrenal cushing’s (kidney)
27
Q
cushing’s disease
A
- pituitary cushing’s - CNS
- pituitary adenoma: secretes ACTH
- ACTH dependent: “disease”
cortisol hypersecretion
28
Q
cushing’s syndrome
A
- adrenal cushing’s - kidney
- adrenal adenoma: secretes cortisol
- exogenous corticosteroids: most common
- iatrogenic cushing’s syndrome - due to medical provider
- ACTH independent: “syndrome”
cortisol hypersecretion
29
Q
cushing’s disease/syndrome - symtpoms
cortisol hypersecretion
A
- central obesity
- rapid weight gain with sparing of limbs
- fat redistribution: moon face, buffalo hump
- skin
- thinning of skin and capillary fragility - easy bruising
- striae
- poor wound healing
- muscle wasting and weakness
- tachycardia, hypertension
- osteoporosis
- impaired GI Ca2+ absorption (antagonizes vitamin D)
- hyperglycemia/DM
- “stress response”
- immunosuppression and increased infection risk
30
Q
treatment of cushing’s disease/syndrome
A
- depends on reason for excess cortisol
- tumor removal: disease (pituitary tumor excision via trans-sphenoidal surgery), sydrome (adrenal tumor excision - adrenalectomy)
- iatrogenic: decrease corticosteroids dosing if possible
31
Q
thyroid gland and function
A
- thyroid follicles produce thyroid hormones (thyroxine T4 and triiodothyronine T3 - ratio is 15:1)
- T4 is a pro-hormone and is converted to active T3 (“the” thyroid hormone)
- iodine necessary for formation of T4 and T3 - goiter is overgrowth of thyroid due to iodine deficiency
- functions
- increase basal metabolic rate (BMR)
- important for brain and muscular development
- CV: increases HR/contractiltiy and cardiac output
- CNS: arousal states
32
Q
thyroid produces calcitonin
A
- calcitonin is produced in response to hypercalcemia - calcitonin decreases serum Ca2+
- calcitonin opposes parathyroid hormone (PTH) - PTH increases serum Ca2+
33
Q
hyperthyroidism
A
- excessive secretion of thyroxine (T4) and/or triiodithyronine (T3)
- common signs and symptoms
- unintended weight loss/diarrhea
- anxiety/nervousness
- heat intolerance
- fatigue/muscle weakness
- palpitations, tachycardia, AFib, hypertension
- tremors
- hyperglycemia
- osteopenia (long term)
34
Q
hyperthyroidism leads to
A
- Graves’ disease:
- autoimmune disease
- thyroid autoantibodies activates TSH-receptor - increase thyroid hormone
- 50-80% of hyperthyroidism (less common pituitary tumor)
- graves’ opthalmopathy (exopthalmos/proptosis) - bulging of eye anteriorly, thyroid eye disease
35
Q
medical treatment for hyperthyroidism
A
- radioiodine therapy: often leads to hypothyroidism
- medications
- thyrostatics (methimazole, propylthiouracil): inhibit iodination of thyroglobulin, inhibit conversion of T4 to T3
- beta blockers
- thyroid surgery
- thyroidectomy: not very common because medical therapy is effective
36
Q
hypothyroidism
A
- common signs and symptoms
- lethargy and fatigue
- bradycardia
- edema
- weight gain
- cold intolerance
- bry skin/brittle hair and fingernails
- goiter
37
Q
parathyroid glands
A
- secretes parathyroid hormone (PTH): breaks down bone, increases Ca2+ in blood
- regulates plasma calcium (osteoclast activity)
- regulates phosphate levels
- most people have 4 on posterior surface of thyroid gland
- chief cells of parathyroid gland produce - parathyroid hormone (PTH)
38
Q
function of PTH
A
- increases blood calcium (Ca2+) concentration when serum Ca2+ is too low (hypocalcemia)
- mechanisms of raising blood calcium
1. stimualtes osteoclasts to release more Ca2+ from bone
2. decreases secretion of Ca2+ by kidney
3. activates vitamin D, which stimulates uptake fo Ca2+ from intestine/diet (vitamin D necessary to absorb Ca2+ in gut) - has opposite effect on calcium as calcitonin (which lowers Ca2+ levels)
39
Q
osteoporosis
A
- systemic skeletal disease characterized by low bone mass and micro-architectural deterioration of bone tissue leading to enhanced bone fragility and a consequent increase in fracture risk
40
Q
osteoporosis risk factors
A
- major modifiable risk factors
- inadequate nutritional absorption - vitamin D deficiency
- lack of physical activity or fall risk
- weight loss
- cigarette smoking
- alcohol consumption (> 2 drinks/day)
- stress - cortisol
- major non-modifiable risk factors
- history of falls
- older age
- gender (women)
- white and asian ethnicity
- prior fracture
- family history of osteoporosis
41
Q
medical conditions associated with increased risk of osteoporosis
A
- prolonged corticosteroid use
- hypogonadism
- hyperparathyroidism
- chronic liver and renal disease
- inflammatory diseases (RA, IBS, MS, COPD)
- diabetes mellitus
- dementia
secondary causes of osteoporosis
42
Q
medical conditions associated with increased risk of osteoporosis
A
- prolonged corticosteroid use
- hypogonadism
- hyperparathyroidism
- chronic liver and renal disease
- inflammatory diseases (RA, IBS, MS, COPD)
- diabetes mellitus
- dementia
secondary causes of osteoporosis
43
Q
all fractures are associated with [ ]
A
morbidity
44
Q
WHO criteria for DXA diagnosis of osteoporosis and FDA-approved drugs
A
- biphosphonates - most common
- selective estrogen receptors modulators (SERMs)
- calcitonin
- parathyroid hormone (PTH)
- estrogen/hormone therapy
45
Q
biphosphenates - antiresorptive agents
osteoporosis drug
A
- mechanism: inhibits bone resorption by attaching to bony surfaces undergoing active resorption and inhibiting action of osteoclasts
- leads to increases in bone density and reduced fracture risk
46
Q
exercise training of individuals with osteoporosis (ACSM)
A
- F: resistance training 2-3 days/week
- intensity: resistance (moderate intensity - 60-80%), aerobic (moderate to vigorous - 40-60%, 60-85%)
- time: 30-60 minutes (> 150 min/week)
- emphasis on extension while avoiding loaded trunk flexion and rottation, supervision for instruction in safe movement
- balance, posture, flexibility
47
Q
diabetes mellitus
A
- 37.3 million people in the US - 11.3% of population
- chronic metabolic disorder characterized by high blood glucose (“hyperglycemia”)
- Type 1
- beta cell of pancreas that produce insulin are destroyed - autoimmune, attacks pancrease
- results in insulin dependence
- commonly detected before 30 YO
- Type 2
- blood glucose levels rise to (1) insufficient insulin action - insulin resistance, then (2) declining insulin production
- common after 40 YO, effects 90% of DM population
- eventually leads to beta cell failure (resulting in insulin dependence)
48
Q
glucose homeostasis
A
- glucose bumps weith meals and in morning due to sympathetic discharge
49
Q
diabetes testing
A
- fasting plasma glucose test (FPG) - cheap, fast
- normal: 70-100 mg/dL (126 + diabetic)
- glycosylated hemoglobin tests (HbA1c) - 90-120 days
- normal: < 5.7% of total Hb
- oral glucose tolerance test (OGTT) - 2 hours after glucose-rich drink
- < 140 is normal, > 200 is diabetic
50
Q
criteria for diagnosis of diabetes
A
- fasting plasma glucose > 126 mg/dl
- 2 hour plasma glucose > 200 mg/dl
- A1C > 6.5%
- classic diabetes symptoms + random plasma glucose > 200 mg/dl
51
Q
complications of diabetes mellitus
A
- cardiovascular disease: CAD, HTN, PVD/peripheral arterial occlusive disease, CVA
- retinopathy
- nephropathy
- neuropathy: polyneuropathy (diabetic peripheral neuropathy [DPN]), cardiac autonomic neuropathy (CAN)
- osteopathy
- immune dysfunction (increased infection risk)
- higher risk for occlusive vascular mortality, coronary heart disease, stroke
52
Q
coronary artery disease (CAD)
DM
A
- CAD/MI is major cause of death in both types of DM (~70%)
- silent ischemia/MI, SOB/DOES, GI symptoms
- increased morbidity and mortality in patients with DM vs non-DM
- atherosclerosis more diffuse throughout coronary arteries (increase HTN, CHF, CVA risk)
- increased incidence of dysrhythmias (VT/MF) post MI - increased mortality
if patient has DM, assume heart disease until prove otherwise
53
Q
retinopathy
DM
A
- early recognition of visual changes and treatment best option for preventing further damage
- affect 80% of patients with DM for > 20 years
- accounts for ~12% of new cases of blindness
- involves macular edema and formation of fragile blood vessels (neovascularization) that may bleed (vitreous hemorrhage)
54
Q
diabetic peripheral neuropathy (DPN) and autonomic neuropathy
A
- DIPN: most common complication of DM type I and II
- sensory - loss of protective sensation
- impacts longer nerve fibers - distal > proximal
- decreased vibration and proprioception
- diminished reflexes: late change
- neuropathic pain
- motor involvement: progressive weakness and atrophy - loss of intrinsics (foot deformity)
55
Q
autonomic neuropathy
DM
A
- same process as DPN but to ANS
- heart and vasculature: orthostatic hypotension, silent MI - no heart pain or pressure
- GI tract: gastroparesis, diarrhea - lose stomach peristalsis and contraction in GI tract
56
Q
osteopathy - charcot’s disease
DM
A
- neuropathic arthropathy
- progressive degeneration of a WB joint
- increase risk of skin breakdown
- varied pressure distribution
- if compined with DPN = increased wound risk
57
Q
MSK system clinical manifestations
DM
A
- upper extremity
- frozen shoulder/adhesive capsulitis
- carpal tunnel syndrome
- flexor tenosynovitis (trigger finger)
- dupuytren’s contraction
- spine
- osteoporosis
- diffuse idiopathy skeletal hyperostosis (DISH) - forestier disease
58
Q
immune function and infection clinical manifestations
DM
A
- innate immunity is impaired
- decreased function of macrophages
- skin breakdown is common
- infections mroe rapidly enter body
- hyperglycemia promotes bacterial growth and proliferation
- glucose “feeds” infection - needs more/longer antibiotics for ulcers because antibiotics never make it through damaged vasculature to infection
59
Q
diabetic ketoacidosis (DKA)
A
- lack of insulin and increased glucagon
- increased release of glucose by liver (gluconeogenesis)
- release of free fatty acids from adipose tissue (lipolysis) that are converted by live to ketone bodies - decrease blood pH
- osmotic diuresis - glucose in urine promotes loss of H20 and electrolytes
- S/S: N/V, abdominal pain, polydipsia, polyuria, dehydration, hypotension
- precipitated by acute illness, MI, CVA, drug abuse, poor DM mangament
DM I > DM II
60
Q
DKA and osmotic diuresis
A
- high glucose concentrations in nephrons draws water into nephrons by osmosis
- leads to excessive urine output (polyuria) and excessive fluid loss (dehydration)
61
Q
glucose and the kidney
DM
A
- glucose freely filtered, not secreted and is usually reabsorbed – so plasma glucose is not “cleared”
- glucose usually appears in urine when serum glucose increases to > 180 mg/dL (> 180 mg/dL reabsoprtion capability of the kidneys - osmotic diuresis)
- excess glucose overwhelms filtering -> glucose in urine: draws water in: polyuria
62
Q
management of DM
A
- major components of treatment of diabetes are:
1. diet and exercise
2. oral hypoglycemic therapy
3. insulin therapy
63
Q
DM management - diet
A
- diet is a basic part of management - treatment cannot be effective unless adequate attention is given to ensuring appropriate nutrition
- aimed at: weight control, providing nutritional requirements, allowing good glycemic control with blood glucose levels as close to normal as possible, correcting any associated blood lipid abnormalities
64
Q
DM management - exercise
A
- exercise promotes weight reduction and improves insulin sensitivity -> lower blood glucose levels
- should be considered with dietary treatment for each person
- educate on hypoglycemia and how to avoid it
150 min/week, 30-60 min per episode. 75% HRM
65
Q
exercises in management of DM I and II
A
- DM I
- improves physical fitness
- increases self confidence
- improves CV function and reduces CV disease risk profile
- no direct effect on glucose control
- DM II
- improves physical fitness
- increases self confidence
- improves CV function and reduces CV disease risk profile
- improves glucose control: improves insulin sensitivity, increases glucose transporters (Glut 4)
66
Q
exercise in DM has [ ] effects
A
- insulin-like effects
- exercise accelerates glucose uptake into peripheral tisssues
- physical activity increases risk of hypoglycemia for hours after
- may need to change insulin dosing with exercise or PT session
- monitor blood glucose before, during, and after exercise sessions
- insulin and exercise: Glut 4 transporter to cell membrane - increases uptake of glucose to lower blood glucose
67
Q
DM exercise guidelines and recommendations
A
- hypoglycemia BG < 60 mg/dl: S/S of HA, confusion, fatigue, hunger, tachycardia, sweating, anxiety
- be aware of nocturnal and post exercise hypoglycemia
- may require lower insulin dose pre-activity or increase carb intake prior to, during, or after activity
68
Q
DM, exercise, and hyperglycemia
A
- postpone “exercise” if blood glucose > 250 mg/dl
- moderate to vigorous intensity exercise
- may lead to exercise induced hyperglycemia: glucagon release with exercise combine with hyperglycemia that can result in ketone bodies and ketoacidosis
mobility is not the same as mdoerate to vigorous exercise
69
Q
other DM and exercise considerations
A
- retinopathy
- avoid strenuous exercise including isometrics, head down positioning, valsalva
- SBP < 50 mmHg above resting
- increased risk of vitreous hemorrhage
- osteopathy and loss of protective sensation
- be aware of potential foot deformities with weight bearing exercises - increased wound risk
- cardiac autonomic neuropathy (CAN)
- may be indicated by resting tachycardia
- angina equivalents/blunted awareness of CP
- postural hypotension
- dehydration
- polyuria and polydipsia
- increase fluid intake throughout exercise session
70
Q
oral hypoglycemic medications
A
- biguanides (metformin): inhibit glucose production in liver
- sulfonylureas: increase insulin secretion
- GLP-1 receptor agonist (ozempic): increases insulin secretion, inhibits glucagon
71
Q
injectable insulin
A
- rapid-acting: 5-15 minute onset, 30-90 minute peak, 3-5 hour duration
- short-acting: 30-60 minute onset, 2-4 hour peak, 6-8 hour duration
- intermediate-acting
- long-acting
72
Q
metabolic syndrome
A
- disorder diagnosed by co-occurrence of 3/5 of the following
1. abdominal (central) obesity (visceral adiposity)
2. elevated BP
3. elevated fasting plasma glucose
4. high serum triglycerides (TG)
5. low high-density cholesterol (HDL) levels - increases risk of developing CO disease, particularly heart failure and diabetes
73
Q
peripheral arterial disease AKA
A
- peripheral vascular disease (PVD)
- peripheral arterial occlusive disease (PAOD)
74
Q
peripheral arterial disease (PAD)
A
- atherosclerotic changes leading to arterial stenosis
- most common symptom is intermittent claudifcation: reproducible ischemic muscle pain with activity and relieved with pain (angina of the leg)
- 10% of men and women > 65 YO
- risk factors: smoking, HTN, atherosclerosis, DM, hypercholestermia, age > 60
75
Q
diagnosis of PAD
A
- vascular studies
- ultrasonography - doppler ultrasound
- magnetic resonance angiography (MRA)
- computed tomographic (CT)
- ABI: can help determine where the blockage is
76
Q
PVD and exercise limitations
A
- inequality between blood flow (supply) and metabolic demand
- produces sensation of burning/ache in calf, thigh, butt
- discomfort subsides with rest - intermittent claudication
- etiology
- muscle ischemia
- structural changes in skeletal muscle: muscle weakness, muscle atrophy, denervation, reduced endurance
77
Q
PAD exercise training prescription
A
- warm-up: 5 minutes
- repeated exercise periods: ends at moderate to severe claudication level
- rest periods: until claudication abates
- frequency: 3-5 supervised sessions/week
- intensity: 35-50 minutes of exercise/session
- type: treadmill of track walking to near-maximal claudication pain
78
Q
T score/Z score scale
A
- highlights bias in system comparing with T score of 30 YO health caucasian woman
- Z-score compares bone density to average bone density of people your own age and gender
79
Q
relative risk vs absolute risk
A
- absolute risk: risk of developing the disease over a time period (1 in 10 risk of developing a certain disease in life - 10%, 0.1)
- relative risk: compares the risk in 2 different groups of people (smokers vs non-smokers)
80
Q
relative risk vs absolute risk
A
- absolute risk: risk of developing the disease over a time period (1 in 10 risk of developing a certain disease in life - 10%, 0.1)
- relative risk: compares the risk in 2 different groups of people (smokers vs non-smokers)
