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
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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
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3
Q

why is the hypothalamus so important

A
  • “master gland”
  • major link between nervous and endocrine system
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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
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5
Q

what does the hypothalamus do

A
  1. 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)
  2. synthesizes 2 hormones that are stored in posterior pituitary
    * oxytocin - the love hormone
    * vasopression (also called antidiuretic hormone (ADH))
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6
Q

releasing hormones

A
  • regulatory hormone from hypothalamus
  • stimulate release of anterior pituitary hormones
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7
Q

release inhibitory hormones

A
  • regulatory from hypothalamus
  • inhibit release of anterior pituitary hormones
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8
Q

hormones stored in posterior pituitary

A
  • oxytocin and vasopression/ADH
  • synthesized by hypothalamus
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9
Q

hypothalamus and anterior pituitary

A
  • hypothalamus produces releasing and inhibiting hormones
  • hypophyseal portal system: connect hypothalamus to pituitary
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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)
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11
Q

hypophyseal portal system

A
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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
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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
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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
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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)
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16
Q

posterior pituitary (neurohypophysis)

A
  • stores releases 2 hormones
    1. ADH (vasopressin): anti-diruetic hormone - increases BP
    2. oxytocin
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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)
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18
Q

does ADH increase or decrease during happy hour

A
  • goes down - pee a lot
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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
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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
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21
Q

adrenal disorders

A
  • hyperfunction
  • Cushing’s disease/syndrome
  • hyperaldosteronsim (Conn’s syndrome)
  • pheochromocytoma
  • hypofunction
  • hypoaldosteronism/hypocortisolism (Addison’s disease)
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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)
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23
Q

normally, as cortisol synthesis increases, what happens to CRH production

A

goes down

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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
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25
Q

osteoblasts vs osteoclasts

A
  • osteoblasts build bone
  • osteoclasts eats up bone
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26
Q

cushing’s disease/syndrome

A
  • hypersecretion of cortisol
  • cushing’s disease - pituitary cushing’s (CNS)
  • cushing’s syndrome - adrenal cushing’s (kidney)
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27
Q

cushing’s disease

A
  • pituitary cushing’s - CNS
  • pituitary adenoma: secretes ACTH
  • ACTH dependent: “disease”

cortisol hypersecretion

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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

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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
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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
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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
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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+
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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)