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Year 3: Clinical Medicine and Pathophysiology > Lecture 5: Metabolic and Endocrine Pathophysiology > Flashcards

Lecture 5: Metabolic and Endocrine Pathophysiology Flashcards

1
Q

key functions of metabolic system

A

convert food to energy

break food down into protein, lipids, carbs, and nucleic acids

eliminate metabolic waste

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2
Q

organs of metabolic system

A

liver
GI tract
pancreas
adipose tissue
muscles

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3
Q

what is catabolism

A

breaking down large molecules into smaller ones

releases energy

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4
Q

what is anabolism

A

combines small molecules into larger ones

requires energy

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5
Q

what is oxidative metabolism

A

energy produced from O2 and glucose

CO2 and water byproduct

aerobic metabolism

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6
Q

what is glycolic metabolism

A

energy produced from proteins and glucose

lactic acid byproduct

anaerobic metabolism

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7
Q

what is Wilson’s disease, common presentation, S&S, and PT implication

A

abnormal metabolism of capper that leads to build up of copper in the liver, kidneys, CNS, and eyes

most common presentations
- liver disease (younger)
- neurological impairments (older pts)

S&S
- liver failure/cirrhosis
- parkinsonian features
- ataxias
- rigidity
- dysarthria
- premature osteoporosis
- CM
- infertility

PT implication = treat neurological S&S in association with medical management

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8
Q

what is Phenylketonuria (PKU)

A

rare inherited metabolic disorder that causes an amino acid to build up bc of the absence of the enzyme that breaks it down

usually diagnosed within first few months of life

most common presentations = severe developmental/intellectual disability

S&S
- gait impairments
- psychiatric difficulties
- abnormal body odor

PT implications = treat developmental delays

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9
Q

what is Paget’s disease: common presentation, S&S, and PT implications

A

metabolic bone disease caused by high bone reabsorption followed by unrestricted bone formation

common presentation = excessive bone formation lacks structure/strength despite appearing hypertrophic; commonly affects long bones

S&S
- repeated fx
- arthritis
- pain
- MSK deformity

PT implications
- resistance train to build bone density and surrounding mm
- awareness of increased risk of fxs
- weight control and cardiac fitness to manage S&S

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10
Q

what is gout/common presentation/incidence

A

acute inflammatory reaction to high concentration of urate crystals in the synovial space of joints

caused by hyperuricemia or too much uric acid in the blood (uric acid metabolized by the kidneys for excretion)

higher prevalence in pts with CKD, HTN, diabetes, HF, obesity, and other metabolic dysfunctions

20:1 make to female

can be diagnosed via blood test or arthrocentesis

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11
Q

symptoms of gout

A

red, inflamed, swollen joint (sometimes unilateral)

very painful

toes, thumb, elbows, knees most common site

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12
Q

PT implications for gout

A

awareness of increased risk of recurrence with PMH of gout

compensatory strategies based on location

ROM to increase synovial fluid production

weight control and cardiac fitness to manage S& S

encourage medical/pharm treatment and compliance

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13
Q

what is osteomalacia, S&S, and PT implications

A

ineffective bine mineralization causing softening of bone

vitamin D deficiency is main cause in adults and impaired calcium absorption

S&S
- bone pain
- proximal mm weakness
- hip/pelvic pain
- fx sometimes is first presenting symptom

PT implications
- weight bearing exercise, but not high impact
- encourage dietary and medical compliance

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14
Q

key functions of endocrine system

A

maintains homeostasis

communicates with CNS to coordinate and integrate cellular activity at different organs/organ systems

controls, correlates, and integrates
- reproduction
- growth/development
- maintenance of electrolytes, water, and nutritional balance of blood
- regulation of cellular metabolism and energy balance
- mobilization of body defenses

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15
Q

components of endocrine system

A

glands
hormones
receptors

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16
Q

what is graves disease

A

autoimmune disorder that causes HYPERthyroidism and excessive thyroid hormone production

strong family hx

clinical presentation
- heat intolerance
- weight loss
- fatigue
- diaphoresis
- anxiety
- irritability
- tachyarrhythmias
- enlarged thyroid (goiter)
- B ptosis w/ eyelid retraction

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17
Q

graves disease treatment

A

radioactive iodine to destroy cells that produce thyroid hormones

antithyroid drugs

Thyroidectomy

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18
Q

PT implications for graves disease

A

tachyarrhythmias, dyspnea on exertion

decreased peripheral mm oxygen extraction

myopathies, proximal mm weakness

heat intolerance

meds/sx management can cause pt to fluctuate between hypothyroidism and hyperthyroidism

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19
Q

what is hypothyroidism

A

low levels of thyroid hormones which control most metabolic functions in body

iodine deficiency is main cause in developing nations

autoimmune disorders are main causes in developed nations (i.e. Hashimotos)

clinical presentation
- fatigue
- weight gain
- decreased metabolism
- hair loss
- dry skin
- cold sensitivity
- constipation

20
Q

medical management of hypothyroidism

A

hormone replacement therapy (lifelong)

treatment of side effects if needed once thyroid levels are normal

21
Q

PT implications for hypothyroidism

A

improve activity tolerance and mm strength/endurance

can only make impact once pt is properly medically managed

increased activity will help negate constipation

edu on management of other S&S and medical compliance

22
Q

what is syndrome of inappropriate antidiuretic hormone secretion (SIADH)

A

too much ADH released by pituitary

kidneys abnormally retain too much water

causes
- medications
- response to GA
- neuro insult
- pituitary tumor
- infections

presentation
- hyponatremia
- hypervolemic but highly concentrated urine
- N&V
- HA
- Vision changes
- balance impairments
- AMS
- other neuro S&S
- seizures

23
Q

PT implications of SIADH

A

awareness of hypoNa

HTN awareness

may need to wait until pt is no longer symptomatic form their hypoNa

edu to pt/family on looking out for worsening S&S

24
Q

what is diabetes insipidus

A

pituitary gland doesn’t release enough ADH

kidneys abnormally produce too much urine w/o ADH signaling to retain normal levels of water

no connection to diabetes mellitus and does not affect blood sugar in any way

causes:
- genetics
- pituitary/other brain tumor
- severe TBI
- hormones with pregnancy
- type of kidney disorders

25
clinical presentation of diabetes insipidus
extreme levels of urine production excessive thirst regardless of intake hyperatremia hypovolemic
26
PT implications of diabetes insipidus
impairment based treatment approach hypotension awareness encourage rehydration
27
what is Addisons disease
adrenal insufficiency; reduced production of cortisol and aldosterone autoimmune disorder that causes progressive destruction of adrenal cortex TB is most common cause adrenal insufficiency from long term corticosteroid use is NOT the same as Addisons presentation: - slow developing weakness/fatigue/back and leg pain - GI distress - weight loss - poor appetite - crave salt - hypoglycemia - hypovolemia - hyponatremia with hyperkalemia - skin hyperpigmentation
28
associated comorbidities with addisons disease
hypothyroidism DM 1 chronic hepatitis osteoporosis
29
PT implications with addisons disease
chronic steroid replacement and accompanying side effects symptomatic treatment of back and leg pain postural control and core strengthening encourage medical compliance
30
what is Cushing's syndrome
over secretion of cortisol by adrenal cortex OR long term use of corticosteroids mist commonly results from long term steroid use seen in pts with cancer, lung diseases, autoimmune diseases, or MS clinical presentation: - moon face - buffalo hump - abdominal obesity - mm wasting/weakness - bone density impairments - skin changes (red cheeks, poor wound healing)
31
PT implications for Cushing's disease
weight bearing exercises, not high impact posture control/core strengthening reduce fall risk wound prevention/healing awareness of side effects of chronic steroid use
32
normal physiology of pancreas
Islets of langerhans in pancreas produce insulin and glucagon insulin ( B cells) suppress glucose production glucagon (a cells) stimulate glucose production lack of insulin results in inability to use glucose as fuel and impaired protein metabolism
33
actions of insulin
facilitates glucose transport across cell membrane for cell metabolism; both oxidative/aerobic and glycolytic/anaerobic enhances cellular utilization and storage of glucose promotes adipose synthesis into amino acids (free fatty acids) enhances utilization of amino acids in liver and throughout body
34
describe type 1 diabetes
progressive destruction of insulin secreting B cells in islets of L result = complete lack of systemic insulin; needs to be replaced pharmacologically 5-10% of DM cases usually diagnosed in 1st 10 years insulin dependent diabetes mellitus = IDDM
35
describe type 2 diabetes
decreased sensitivity to circulating insulin glucose doesn't get transported through cell membranes to be stored for energy in mm/liver/fat = too much blood glucose 90-95% DM cases usually happens in adulthood, but trending younger ages now non-insulin dependent diabetes mellitus = NIDDM
36
S&S of DM type 1 vs type 2 that are DIFFERENT
DM 1 - N&V - constant hunger - sweet breath DM 2 - yeast infections - slow wound healing
37
CVP complications from DM
increased risk for: - CAD/HF/HTN (5x greater risk for some type of heart disease) - PAD - SVA - autonomic dysfunction - thickened alveolar membrane - systemic microvascular disease, common in kidneys and eyes indirect relation to: - reduced peripheral O2 extraction - higher CV fitness needed for some tasks - increased blood viscosity
38
microvascular diseases that can be of diabetic origin
diabetic: - CM - neuropathy - retinopathy - encephalopathy - neuropathy
39
blood glucose lab values
immediate reading of blood sugar normal = 70-100 mg/dL 140-199 = pre diabetes >200 = diabetes
40
hemoglobin A1c lab values
glucose adheres to RBCs for 3 month lifespan; HgbA1c = average measurement of BS over 3 month period normal = <5.7% 5.7-6.4% = prediabetes >6.5% = diabetes
41
what is hypoglycemia
too much insulin, not enough glucose BS <70 SNS activation S&S - tremors - anxiety - tachycardia - diaphoresis - AMS - dizziness - blurred vision - hunger - seizures need easily absorbed glucose ASAP
42
what is hyperglycemia
too much glucose, not enough insulin BS > 300 inadequate insulin levels more common in DM2 S&S - frequent urination w high glucose content - dehydration - thirst/hunger - HA - blurred vision - N&V - SOB - dry mouth - AMS
43
what is diabetic ketoacidosis (DKA)
insufficient insulin to allow blood glucose from entering cells alternative source = liver breaks down fat and produces ketones ketones build up in blood = high glucose and low insulin more common with DM1 or uncontrolled DM 2 S&S - tachycardia - HTN - severe SOB - dehydration - uncontrolled vomitting - abdominal pain - sweet breath - electrolyte abnormalities medical emergency requiring insulin infusion
44
exercise impact on DM
PA reduces insulin secretion compensated for by increased peripheral sensitivity = more rapid glucose uptake by mm helps decrease BS and HgbA1c resistance training more effective when targeting major mm groups with high intensity strength training (3 sets, 8-10 reps, weight near fatigue, 3x/wk)
45
what type of exercise causes mm to have increased glucose uptake for energy production as well as reduces hyperglycemia in DM pts
low-moderate intensity
46
best exercise type to provide benefits on HgbA1c
combined aerobic and resistance

Year 3: Clinical Medicine and Pathophysiology (8 decks)

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