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endocrine Flashcards

1
Q

adipokines

A

regulate food intake and metabolism
increase or decrease fat mass, provide signals to the hypothalamus, brainstem, ANS and hunger center to regulate satiety and energy balance

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2
Q

obesity

A

metabolic disorder- increase in adipose tissue
BMI> 30
increases risk of HTN, stroke, HLD, cholelithiasis, fatty liver, GERD, hiatal hernia, osteoarthritis, infectious disease, asthma, OSA, and CDK
genetic predispositions from: metabolic disorders like Cushings, PCOS, growth hormone deficiency, hypothyroidism, hypothalamic injury
socioecomonic factors contribute as well

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3
Q

White Adipose Tissue (WAT)

A

increases in size and number
stores triglycerides
secretes adipokines
visceral WAT causes a dysfunction in regulatory signaling center and leads to the complications associated with obesity

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4
Q

hypothalamus affect on food intake

A

regulates food intake and energy balance by regulating neurons which increase and decrease appetite

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5
Q

adipose tissue-gut-brain axis

A

GI tract releases adipokines and hormones which interact with the brain and contribute to the patho of obesity

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6
Q

Leptin

A

produced by obesity gene (Ob gene)

  • high levels inhibit the appetite by blocking neurons that increase the appetite
  • leptin levels increase when adipocyte numbers increase
  • can lead to leptin resistance
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7
Q

leptin resistance

A

promotes over-eating and weight gain

  • leads to hyperglycemia, increased insulin secretion, HLD, release of proinflammatory mediators
  • chronically elevated leptin levels promote chronic inflammation, ventricular hypertrophy, HTN, atherosclerosis, CV disease, cancer, insulin resistance
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8
Q

adiponectin

A

mainly secreted by viseral adipose tissue, it increases insulin sensitivity and has anti-inflammatory properties

  • levels decrease in obesity
  • leads to insulin resistance, development of type 2 diabetes, increase in hepatic gluconeogenesis, decreased skeletal muscle glucose uptake, increased levels of inflammatory mediators
  • increased risk of CAD, chronic inflammation and thrombosis
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9
Q

endocannabinoids

A

derived from arachidonic acid

-increase appetite, enhance nutrient absorption, stimulate lipogenesis, increase WAT, inhibit energy expenditure

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10
Q

angiotensinogen

A

made by liver and adipocytes

  • increased in obesity
  • precursor to angiotensin I, which leads to angiotensin II
  • angiotensin II causes vasoconstriction, renal retention of Na and water and aldosterone
  • leads to inflammation, lipogenesis, oxidative stress, and insulin resistance > all assoicated with HTN, atherosclerosis, DM 2 and cancer
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11
Q

Ghrelin

A

produced by gastric mucosa in response to hunger and stimulates food intake

  • increases body weight and body fat
  • stimulates growth hormones, release of gastric acid, GI motility and insulin secretion
  • promotes satiety, vasodilation and is cardioprotective
  • NORMALLY increases and then decreases after eating
  • in obesity, levels are lower and there is a blunt response to eating
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12
Q

glucagon-like peptide 1

A

secreted by endocrine cells of the intestine

  • stimulates insulin secretion, delays gastric emptying, suppresses the appetite and increases energy use
  • levels are decreased in obesity
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13
Q

peptide YY

A
  • released from endocrine cells in intestines
  • inhibits gastric motility and decreases a person’s appetite
  • levels are decreased in the obese
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14
Q

viseral obesity

A

accumulation of adipose tissue in the abdomen and upper body

-assoicated with chronic inflammation, metabolic syndrome, OSA, DM2, CV disease, osteoarthritis, fatty liver and cancer

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15
Q

peripheral obesity

A
  • “pear shaped”
  • fat accumulates in thighs and buttocks
  • releases less adipokines than viseral fat
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16
Q

aging related changes to endrocine system

A
  • thyroid gland atrophies and fibroses, thyroid disease is more common in elderly
  • TSH secretion increases slightly
  • pancreas beta cell function declines> glucose intolerance or DM
  • growth hormone secretion decreases> decrease in muscle size and function, decreased amounts of fat and bone mass, changes in reproductive and cognitive function
  • elevated PTH> increase mortality
  • decreased vitamin D levels> osteoporosis, cancer, autoimmune disorders, DM, CV disease, mental health
  • after 50, adrenal cortex fibroses
  • cannot clear glucocorticoids very well> circulating levels increase
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17
Q

anorexia of aging

A
  • decrease in appetite or food intake in elderly
  • leads to malnourished state and adverse outcomes
  • results from: reduced energy requirements, diminished hunger, decreased sense of taste and smell, decreased saliva secretion, altered GI satiety control mechanism, neuronal changes that suppress appetite, chronic inflammation
  • risk factors: functional deficits, medial/psych conditions, loneliness and grief, meds, polypharmacy, social isolation, abuse or neglect
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18
Q

anorexia of aging adverse outcomes

A
  • malnutrition
  • physical frailty
  • mitochrondrial dysfunction
  • reduced regenerative capacity
  • increased oxidative stress
  • imbalanced hormones
  • increased mortality
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19
Q

thyroid A & P

A
  • thyroid secretion is regulated by TSH which is released from anterior pituitary
  • most of hormone is released as T4 (90%) and T3 (10%)
  • T3 & T4 have same functions, but T3 is more potent
  • prior to entering nucleus of cell, T4 is converted into T3
  • both hormones bind to thyroxine-binding globulin (TBG) or albumin in blood (function as transport proteins)
  • T3 & T4 are stored as thyroglobulin (TG) which is a precursor to both hormones
  • enough stored to last 2-3 months
  • low levels of thyroid hormones stimulate the release of thyroid-releasing factor which stimulates the release of TSH, which stimulates the release of T3 & T4
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20
Q

thyroxine formation

A

formed with iodine

  • iodides used to make thyroxine are trapped by thyroid gland
  • uptake of iodine is regulated by TSH
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21
Q

T3 & T4 functions

A
  • increase metabolism
  • maintain muscle tone
  • skeletal muscle maturation
  • antagonization of insulin
  • regulation of cellular metabolism
  • promote production of heat
  • maintain CO, contraction and rate
  • maintain GI secretion
  • calcium mobilization and stimulation of lipid metabolism
  • free fatty acid release
  • cholesterol synthesis
  • RBC production
  • affections respiratory rate and O2 utilization
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22
Q

thyroid hormone effects on the heart

A

T3 stimulates the production of

  • the contractile protein a-myosin heavy chain
  • the sarcolemma ion pumps
  • B-adrenergic receptors
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23
Q

calcitonin

A

secreted by C-cells of thryoid

  • lowers serum calcium by preventing bone resorption effects of PTH, prostaglandins and calciferols by blocking osteoclastic activity
  • lowers phophate levels
  • decreases GI absorption of calcium and phosphorous
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24
Q

hyperthyroidism

A
  • from over-secretion of thyroid hormone
  • can be caused by Grave’s disease, thyroid cancer, or thyroid nodules
  • CM: metabolic rate increases, heat intolerance, goiter, menstrual irregularities, weight loss, diaphoresis, fine tremor, tachycardia, frequent BMs, restlessness, short attention span, hair loss, anorexia, exophthalmos, pretibial edema, HF
  • labs will show low TSH and high T4
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25
Q

Grave’s disease

A

autoimmune disease

  • more common in women than men
  • antibodies attach to thyroid cells and mimic the function of TSH, which increases secretion of T3 & T4
  • overrides the negative feedback mechanism which regulates TSH secretion
  • leads to development of goiter, exophthalmos, periorbital edema, extraocular muscle weakness (leads to strabismus and diplopia)
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26
Q

thyroid nodules

A

cause hyperthyroidism

  • follicular hypertrophy of thyroid cells leads to nodule formation
  • can develop becuase of normal changes during pregnacy or puberty, autoimmune issues, viral infections or genetic influences
  • symptoms develop slowly: do not experience exophthalmos and pretibial myxedema (plaques develop on skin)
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27
Q

thyroid storm (thyrotoxic crisis)

A
  • dangerous worsening of hyperthyroid state
  • severe and may cause death if not treated
  • triggered by event: infection, trauma, cardiopulmonary disorder, burns, seizures, surgery, or spontaneously
  • extreme restlessness, agitation, delirim, seziures, coma, severe tachycardia, HF, hyperthermia, volume depletion, N/V/D
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28
Q

hypothyroidism

A

-insufficient thyroid hormones
-more common in women and elderly
-primary or secondary
-CM: confusion, syncope, slow speech and thinking, memory loss, depression
CV: anemia, bradycardia, decreased SV, decreased CO, increased PVR, prolonged PR interval, inverted T waves, cardiac tamponade
Pulmonary: dyspnea, hypoventilation, CO2 retention
decreased appetite, weight gain, coarse hair, dry skin, cold intolerant, low body temp
constipation, HLD, decreased nutrient absorption
periorbital edema, peripheral edema
myxedema (puffy face)
reduced renal blood flow and GFR, increased total body water, hyponatremia
LABS: high TSH and low T3 & T4

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29
Q

primary hypothyroidism

A

primary defect is in thyroid gland
-causes: congenital defects, thyroidectomy, thyroid raditiation, iodine deficiency, anti-thyroid meds, impairment in thyroid hormones synthesis, autoimmune (hashimotos thyroiditis)

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30
Q

secondary hypothyroidism

A

malfunction in pituatary or hypothalamus, leads to lack of TSH
-causes: pituitary tumor (most common), TBI, SAH, pituitary infarction

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31
Q

myxedema coma

A

thyroid emergency (opposite of thyroid storm)

  • decreased LOC (gradual or sudden), hypotension, hypoventilation, shivering, hypothermia, lactic acidosis, coma, hypoglycemia
  • triggering event: infection, DC’d thyroid meds, narcotic or sedative use
  • elderly with UTI, HF, stroke and moderate or untreated hypothyroidism are at increased risk
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32
Q

pancreas basics

A
  • has digestive and endocrine functions
  • contains islets of Langerhans
  • 4 types types of cells: 1) alpha cells secrete glucagon, 2) beta cells secrete gastrin, 3) data cells secrete gastrin & somatostatin, 4) F cells secrete pancreatic polypeptide that stimulates the secretion of gastric acid and inhibits cholecystokinin secretion
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33
Q

proinsulin

A
  • proinsulin synthesizes insulin in beta cells
  • composed of A peptide, B peptide and C peptide
  • C peptide cleaves from complex and can be measured in the blood to determine how much insulin is being secreted
34
Q

insulin secretion

A
  • occurs when beta cells are stimulated by PNS, typically before a meal
  • may also be stimulated by elevated glucose levels, amino acids, GI hormones (glucagon, gastrin, secretin & cholecystokinin)
  • insulin levels drop because of SNS stimulation of beta cells, low glucose levels, high insulin levels and prostaglandins
35
Q

function of insulin, factors that impact insulin sensitivty and insulin resistance

A
  • insulin binds with cell receptors and triggers the activation of glucose transporters (GLUT) to move glucose into the cell
  • GLUT4 is the main transporter> 21 fold increase in glucose diffusion into the cell
  • especially true in skeletal muscles, cardiac muscle, liver and adipose cells
  • age, weight abdominal fat, activity levels all impact insulin sensitivity
  • insulin resistance is associated with HTN, heart disease and DM2
36
Q

amylin

A

hormone secreted by beta cells

-helps to regulate glucose concentration by delaying gastric emptying and suppressing glucagon secretion

37
Q

glucagon

A
  • antagnoizes insulin and increases blood glucose levels during times of fasting, exercise and hypoglycemia
  • stimulates glycogenolysis in the liver
  • glucagon secretion is stimulated by amino acids like alanine, glycine and asparagine
  • glucagon secretion is stimulated by protein rich meal
  • glucagon initiates lipolysis
38
Q

pancreatic somatostatin

A

regulates alpha and beta cells of the pancreas by inhibiting insulin and glucagon

39
Q

glucagon-like peptide 1 (GLP-1) & glucose dependent insulinotropic polypeptide (GIP)

A

control the levels of glucose after one eats by stimulating glucose dependent insulin secretion, inhibiting glucagon synthesis, slowing gastric emptying, and stimulating hepatic glucose secretion

  • increase the intracellular insulin stores
  • GLP-1 receptor agonist is a diabetes drug
40
Q

diabetes

A
  • metabolic disorder marked by hyperglycemia & an alteration in protein and fat metabolism
  • results from pancreatic issues or lack of response to insulin in cells
  • 4 types: DM 1, DM 2, secondardy DM, gestational DM
41
Q

diagnostic criteria for DM

A
  • hemoglobin A1C> 6.5%
  • fasting glucose of > 126 (no caloric intake for 8 hours)
  • two hour plasma glucose tolerance test of >200
  • symptoms of diabetes with a random plasma glucose of >200
42
Q

lab values indicating prediabetes

A
  • hemoglobin A1C 5.7-6.4%
  • fasting glucose 100-125
  • 2 hour glucose toleratance test of 140-199
43
Q

diabetes type 1

A
  • typically diagnosed before age 30, mostly diagnosed between 9 months- 12 years
  • 3 types: 1a: autoimmune related, 1B: idopathatic or non immune and type 3c: chronic pancreatitis
44
Q

Diabetes type 1a

A

t cell mediated autoimmune repsonse that destroys beta cells of pancreas

  • no insulin is produced
  • low insulin levels lead to increased glucagon secretions which increases glycogenolysis and gluconeogenesis
  • also decreases amlyin secretion
  • alters the metabolism of fat, carbs and proteins
  • glucose exceeds renal threshold and spills over into urine and causes osmotic diuresis, polyuria and polydipsia
  • tend to have flucuating glucose levels
  • go into ketosis due to lack of insulin and have muscle and fat breakdown, leads to weight loss
  • may lead to DKA
  • experience polyphagia because of the depeltion of carbs, fats and proteins which are used for energy
45
Q

diabetes type 2

A
  • much more common than type 1
  • onset typically around middle age, but kids are getting it more and more
  • risk factors: HTN, physical inactivity, family history
  • patho: insulin resistance due to decrease in number of insulin cell receptors or insufficent amounts of insulin secretion
46
Q

metabolic syndrome

A
  • prediabetic state
  • central obesity, dyslipidemia, prehypertension, elevated blood glucose levels
  • high risk for development of DM type 2 and cardiac events
47
Q

diagnostic criteria for metabolic syndrome

A
  • waist circumference >40 inches in men and >35 inches in women
  • triglyceride levels > 150
  • HDL <40 in men or <50 in women
  • blood pressure >130/85
  • fasting glucose >100
48
Q

contributing factors to insulin resistance

A
  • obesity: increases serum levels of leptin, decreased levels of adiponectin & inflammation, decreased insulin synthesis, and insulin resistance
  • alpha cells in pancreas are less responsive to glucose inhibition, which increases levels of glucagon and blood sugar levels
  • deficiency in amylin: increases glucagon levels
  • decreased levels of ghrelin: increases insulin resistance and increass fasting insulin levels
  • beta cells response to incretins (GLP-1 and GIP) is reduced in prediabetes in DM 2
49
Q

clinical manifestations of diabetes type 2

A
  • mild polydipsia, polyphagia and polyuria
  • no signs of metabolic acidosis
  • glucose can go much higher (>400-900)
  • fatigue
  • prurtsis
  • recurrent infections
  • neuropathy
  • visual changes
  • weight loss
50
Q

secondary diabetes

A

describes DM which has a clear etiology but not related to type 1 or type 2
-causes: pancreatic disease like cancer or pancreatitis, steroid use, Cushing syndrome, acromegaly, & excess glucagon secretion

51
Q

gestational diabetes

A
  • hyperglycemia appears during pregnancy
  • high risk women who have signs of diabetes on their first prenatal visit should recieve diagnosis of DM 1 or DM 2
  • all women should be screened between 24-28 weeks
  • women with gestational diabetes should be screened at 6-12 weeks postpartum
  • risk factors: obesity, family history of DM, high maternal age
  • usually resolves after birth
  • increased risk of developing DM later in life
  • upon birth, child may have hyperplasia of pancreatic islet cells and hypoglycemia
52
Q

acute complications of diabetes

A
  • hypoglycemia (<40 in newborns, <70 in adults), often caused by insulin therapy or not eating
  • symptoms of hypoglycemia: pallor, tremors, anxiety, tachycardia, palpitations, diaphoresis, HA, dizziness, irritability, fatigue, poor judgement, confusion, seizures and coma (symptoms from release of epinephrine & cortisol during hypoglycemic episode- beta blockers may block many symtpoms)
  • DKA
  • HHS
53
Q

diabetic ketoacidosis (risk factors and common predisposing factors)

A
  • life-threatening, acute complication from insulin deficiency and the release of counter regulatory hormones (catecholamines, glucagon, cortisol)
  • more commonly seen in DM 1
  • most common predisposing factors: concurrent illness, infection, trauma, surgery, MI and lack of medication compliance
  • risk factors: DM type 1, poor glycemic control, younger or older age, ethnic minority, lack of health insuracne, lower BMI, infection, and delayed treatment
  • lack of insulin causes an increase in hepatic glucose production, a decrease in peripheral glucose utilization and the initiation of glucoenogenesis and the formation of ketone bodies and metabolic acidosis
  • may lead to comatose state
54
Q

diagnostic criteria for DKA

A
  • glucose >250
  • serum bicarb <18
  • serum pH <7.3
  • elevated anion gap
  • presense of urine or serum ketones
  • fluid volume deficit
  • electrolyte imbalance
55
Q

treatement for DKA

A
  • IV fluids, IV insulin and treatment of electrolyte imbalances
  • search for cause
56
Q

Hyperosmolar Hyperglycemic State (HHS)

A
  • uncommon complication of type 2 DM
  • more common in elderly
  • triggered by infection, CV or renal disease
  • patho is same as DKA without the production of ketone bodies
  • elevated glucose causes a high osomtic pressure & osmotic diuresis which leads to severe dehydration, low blood volume and poor perfusion
57
Q

HHS diagnostic criteria

A
  • glucose > 600
  • normal bicarb (23-30)
  • osmo > 320
  • absent or low levels of ketones
58
Q

chronic complications of diabetes

A
  • results from toxic effects of glucose
  • artherosclerosis of large and small vessels
  • macroangiopathy: medium and large vessels are damaged by glucose- brain, heart, aorta, femoral arteries: leads to PVD, cerebral atherosclerosis, CAD
  • microangiopathy: small vessel damage, directly related to duration of disease. issues manifest around 10 years post diagnosis. causes thickening of capillary membrane, endothelial cell hyperplasia and thrombosis, all decrease perfusion. can cause damage to retinal arterioles, kidneys (CKD), skin (poor wound healing)
59
Q

angiopathic ischemia & oxidative stress from diabetes causes:

A
  • peripheral neuropathy
  • autonomic neuropathy: damage to nerves of ANS, results in gastoparesis, bladder control problems, silent MI
  • decreased phagocytic action, increases risk of infections
60
Q

adrenal cortex A & P

A
  • secretes glucocorticoids, mineralocorticoids, and gonadocortcoids
  • makes up 80% of glands weight
  • stimulated by ACTH, secreted by anterior pituitary
61
Q

types of glucocorticoids and their actions

A
  • cortisol, corticosterone, and cortisone
  • have effects on metabolism, provide anti-inflammatory properties and growth-suppressing effects
  • inhibit cellular uptake of glucose
  • stimulate gastric acid secretion
  • a metabolite of cortisol acts like a barbiturate and depresses nerve cell function in brain
62
Q

mineralocorticoid example & action

A
  • aldosterone
  • sodium regulation
  • increases renal reabsorption of sodium and decreases renal reabsorption of potassium
  • controlled by RAAS
  • ACE inhibitors have a side effect of hyperkalemia
63
Q

adrenal medulla A & P

A
  • secretes catecholamines, epinephrine, norepinephrine, and dopamine
  • innervated by SNS and PNS
  • cathecholamines increase BP, HR, and cause vasoconstriction
  • also increase RR, glucose levels and cellular metabolism
64
Q

Cushing’s Syndrome

A
  • chronic over-secretion of cortisol
  • most common in elderly & women
  • etiologies: exogenous steriod use, over-secretion of ACTH secondary to pituitary tumor, ectopically produced ACTH from a non-pitutary carcinoma or adrenal adenoma
65
Q

increased levels of cortisol cause: (cushing’s syndrome)

A
  • increased glycogenolysis & gluconeogensis (results in hyperglycemia, insulin resistance and DM 2)
  • abnormal lipolysis and redistribution of fat to other areas of the body and elevated blood lipid products
  • body changes: truncal obesity, moon face, formation of buffalo hump (called cushingoid appearance)
  • elevated LDLs and increased risk of atherosclerosis
  • abnoramlly catabolized protein causes muscle wasting and weakness
  • growth retardation in children
  • breakdown of bones- high urine Ca levels and increased risk of renal stones, osteoporosis and pathological fx
  • weakened collagen fibers (skin fragility)
  • increased anti-immune and anti-clotting effects (inhibition of arachidonic acid pathway)
  • decreased protection of gastric protective prostaglandins (COX 1)
  • peripheral vasoconstriction and HTN (increased catecholamine sensitivity)
  • increased ACTH stimulation to adrenal cortex to over secrete androgens (hirsutism: increased hair growth, and acne)
66
Q

addison’s disease

A
  • decreased levels of cortisol & alderstone secretion
  • occurs most freq between ages 30-60
  • more common in women
  • patho: autoimmune reaction which targets the adrenal cortext and causes adrenal atrophy and hypo function
  • may be caused by TB, metastatic tumors, infections, HIV, fungal infections, amyloidosis or cessation of steriod therapy
67
Q

addison’s disease clincial manifestations

A
  • hypoglycemia- weakness, fatigue, apathy, mental confusion, anorexia, N/V/D, abdominal pain and
  • addisonian triad: hyperkalemia (not enough aldosterone to get rid of K) hyponatremia (not enough aldosterone to keep sodium), hypotension (not enough cortisol to maintain vascular tone)
68
Q

mineralocorticoid deficiency symptoms

A

-hypovolemia, postural hypotension, dizziness, dehydration, hyperkalemia, and salt cravings

69
Q

addisonian crisis

A
  • emergent condition from lack of cortisol and aldosterone

- severe hypotension and vascular collapse

70
Q

osteoporosis

A
  • most common bone disease
  • marked by low bone mineral density, impaired stuctural integrity, decreased bone strength
  • increases risk of fractures
  • primary (idiopathic) & secondardy (caused by another condition)
  • conditions include hormone imbalances, DM, hyperparathyroidsim, hyperthyroidism, heparin, corticosteroids, phenytoin, barbiturate, lithium, tobacco, ethanol, HIV, rhumatoid disease, CDK, liver disease, malabsorption syndromes
71
Q

bone density classifications

A

normal bone mass > 833 mg/cm

osteopenia: bone mass of 648-833 mg/cm
osteoporosis: bone mass <648 mg/cm

72
Q

osteoporosis progression

A
  • progresses slowly
  • person typically only knows they have it after sustaining a fx
  • bone is being broken down faster than it is being made so the bone becomes porous and thin
  • spontaneous fx occur, and from falls or bumps
  • more common in women, >50 years old
  • vertebral fx are most common
73
Q

bone homeostasis

A
  • dpendent upon the balance between cytokine receptor activator of nuclear factor (RANKL), it’s receptor RANK and it’s decoy receptor osteoprotegerin (OPG)
  • osteoblasts express RANKL > RANKL activates RANK receptors which is expressed on osteoclasts > OPG mitigates the process by acting as a decoy receptor and preventing RANKL from binding to RANK
  • process is regulated by hormones and cytokines
  • alteration in this system leads to osteoporosis, immune mediated bone diseases, malignant bone disorders and inherited skeletal diseases
  • estrogen stimulates OPG secretion
  • post menopausal women express higher levels of RANKL, which leads to osteoporosis
  • glucocorticoids increase RANKL expression and inhibit OPG production
  • age related bone loss occurs from decreased levels of growth hormone, increased RANKL activity and decreased OPG function
74
Q

osteoarthritis

A
  • very common form of joint disease
  • leading cause of disability
  • loss of articular cartilage and destruction of the joint capsule
  • may occur secondary to aging or from long term mechanical stress from sports, obesity, chronic diseases like DM
  • women > men
  • > 50 years old
  • joints most commonly affected: hips, knees, lower lumbar, cervical veretbrae, proximal and distal interphalangeal joints of fingers
75
Q

pathological hallmark of OA

A
  • degeneration of the articulating cartilage
  • leads to increased remodeling of the cartilage, loss of smooth, frictionless joint
  • eventually requires joint replacement surgery
76
Q

Clinical manifestations of OA

A
  • dependent upon affected joint
  • pain and stiffness
  • joint swelling, tenderness and deformity
  • symptoms are worsened with weight bearing or joint use and are relieved with rest
77
Q

sarcopenia

A
  • loss of muscle mass secondary to aging
  • loss of Type 2 fiber and a loss of satellite cells
  • reduced RNA synthesis, loss of mithochrondrial volume, shortening telomeres, and a reduction in the size of motor units
78
Q

Duchenne Muscular Dystrophy

A
  • x- linked genetic disorder
  • most common form of MD
  • mainly affects men
  • deletion of one or more exons of the DMD gene on the X chromosome
  • lack of dystrophin allows for muscle fibers to be torn apart during contraction
  • free Ca enters the muscle cells and causes cell death
  • cellular destruction leads to increased levels of CK
79
Q

DMD clinical manifestations

A
  • first noticed around ages 3-4 with a gait abnormaility
  • child will have toe walk, difficulty getting up from the ground and experience frequent falls
  • muscle weakness starting in pelvic area, and have calf muscle hypertrophy
  • display Gwer sign, have progressive weakness and are unable to ambulate by 12-15
  • slow progression leads to respiratory insufficiency, cardiomyopathy, scoliosis and orthopedic complications
  • will have cognitive defects
  • most live into their 20s and die from pulmonary infections
80
Q

DMD gene normal physiology

A
  • makes a membrane stabilizing protein called dystrophin

- anchors the actin cytoskeleton of the skeletal muscle to the basement membrane

Advanced Patho (2 decks)

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