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427 Cards in this Set
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Normal fasting glucose
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100
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Diabetes fasting glucose level
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>126
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DM is the leading cause of what 2 chronic complications
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blindness, end stage renal disease
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3 possible causes of DM
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decreased/no insulin secretion, defective insulin receptors (non-sensitve tissues), or early insulin destruction
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Normal value for oral glucose tolerance test
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<140
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Prediabetes value for fasting plasma glucose
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100-125
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Prediabetes value for tolerance test
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140-199
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DM value for tolerance test
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>200
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Type 1A diabetes
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95% of Type 1 diabetes cases; immune-mediated destruction of B cells; genetically inherited
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Type 1B diabetes
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idiopathic destruction of B cells
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Type 2 DM
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peripheral insulin resistance; 90% of diabetics; glycolysis begins b/c no glucose in the cells, fasting hyperglycemia with insulin availability
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etiology of Type 2 DM
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genetic, environmental
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factor increasing insulin resistence of Type 2 diabetics
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Central/Abdominal obesity; increased free fatty acids in circulation, leading to B cell exhaustion
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Type 2 DM; Metabolic syndrome/ Syndrome X/ Insulin resistence syndrome
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increased triglycerides, low HDL, HTN, increased CRP, abnormal fibrinolysis (increased clots), vascular disease (peripheral, cerebral, coronary)
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Dx of T2DM Met. syndrome
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central obesity, BP>130/85, triglycerides >150, low HDL (men<40, women <50), fasting glucose >110
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Central obesity
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Men >40 in. waist
Women >35 in. waist |
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Risks for gestational diabetes
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family Hx of DM, heavy @ date baby, 5>pregnancies, Hx of still birth or fetal abnormalities
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gestational diabetes complications
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increased risk of maternal/fetal demise, increased risk of fetal abnormalities
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fetal abnormalities associated with gestational diabetes
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macrosomia, hypoglycemia, polycythemia, hypocalcemia, hyperbilirubinemia
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Manifestations of both T1 & T2 DM
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hyperglycemia, polydypsia, polyuria, somnolence, fatigue, blurred vision
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Dx of DM
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FRG >126, casual blood glucose >200 (with 3 P's- polyphagia, polyuria, polydypsia), ITG>200, glycosylated Hgb >6%
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DKA
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mostly in T1 DM; hyperglycemia, glycosuria, increased lipolysis
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causes of DKA
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severe stress -> increased cortisol, epinephrin, glucagon; infection, pregnancy
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Manifestations of DKA
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BGL >250-300, CO2<21, pH<7.35, osmotic diuresis (shock, coma, hypotensive), hypokalemia, glycosurea, ketonuria, fruity breath
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HHNK
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mostly T2DM; BGL>600; insidious, no ketosis
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Manifestations of HHNK
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hyperosmolar >310 (Norm 285), severe dehydration, decreased sensorium, coma, hyperthermia (b/c decreased H20), seizure
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hypoglycemia values
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BGL <50-60
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Manifestations of hypoglycemia
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h/a, abnormal sensorium, "weird feeling", difficulty problem solving, increased norepi, epi, cortisol-> diaphoresis, shaking, palpitations, tachycardia
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Normal glycosylated Hgb
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4-6%
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Microangiopathy
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chronic DM complications; thickening of capillary basement membrane; retinopathy, nephropathy, neuropathy
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retinopathy
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microaneurysms in retinal arteries cause hemorrhage, scarring, and blindness
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nephropathy
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most commonly associated with end stage renal disease, esp. if HTN exists in addition to DM
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neuropathy
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hyperglycemia -> increased intracellular sorbitol -> schwann cell damage, decreased conduction along nerves
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Manifestations of neuropathy
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pain, burning, parasthesias, decreased proprioception, decreased vibratory sense, decreased deep tendon reflexes
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Macroangiopathy
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CAD, peripheral vascular damage, hyperglycemia, hyperlipoproteinemia
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Polyol pathway
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normally, glucose is metabolized to sorbitol, which is them metabolized to fructos; in DM, sorbitol cannot be totally converted to fructose, build-up alters the membrane and function of: eyes, kidnesy, nerves, and vessels
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cause of risk for ulcers and burns
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low Q (perfusion) in tissue, lost sensory/feeling
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Autonomic DM manifestations
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impaired vasomotor control, gastroparesis, impaired geitourinary function
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gastroparesis
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incomplete stomach emptying, related to diarrhea after eating
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cause for hypo- endocrine disorder
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congenital defect, gland destruction, aging/atrophy, receptor defect, impaired responsiveness
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cause for hyper- endocrine disorder
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excessive stimulation, hyperplasia, ectopic source (hormone-producing tumor)
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primary endocrine disorders
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target gland that produces the hormone is defective
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secondary endocrine disorders
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normal functioning target glad, problem is with stimulating hormone/releasing factor
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tertiary endocrine disorder
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hypothalamic dysfunction; both secondary and target organ are understimulated
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GH/somatotropin
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produced by anterior pituitary
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effects of GH/somatotropin
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bone & muscle growth; cartilage, linear bones, stimulates liver to release IGH, increased skeletal/cardiac muscle, skin, connective tissue, increased protein synthesis, fat metabolism, decreased CHO metabolism
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etiology GH deficiency- children
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idiopathic, decreased GnRH, pituitary tumor, congenital defect
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manifestations of child GH deficiency
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normal birth length, slow growth rate, normal intelligence, short stature, obesity, immature facial features, high LDLs; may delay puberty, microphalus, hypoglycemia, decreased ACTH, decreased HDLs
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etioloty GH deficiency- adults
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hypopituitarism (tumor, tumor treatment), somatopause (normal decrease in GH w/age)
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manifestations of adult GH deficiency
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increased risk for CVD-> increased LDL, decreased HDL, increased body fat, decreased body mass
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etiology of GH excess in children
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benign pituitary adenoma
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manifestation of child GH excess
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giantism
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etiology of GH excess in adults
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somatrope adenoma (95%), small cell carcinoma, hypthalamic tumor secreting excess GHRH
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manifestation of excess adult GH
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acromegaly; increased growth of connective tissue and cartilage; insidious
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acromegaly
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bone overgrowth, enlarged feet/hands/face, bulbous nose, protruding jaw, slanted forehead, splayed teeth, kyphosis, arthralgia, deep voice (enlarged larynx), bronchitis, enlarge heart, accelerated atherosclerosis, heat intolerance, menstrual irregularities, fatigue, sleep apnea
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metabolic complications from adult GH excess
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increased FFA circulation, altered CHO metabolism; insulin resistence, B cell burnout
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effects of T3/T4
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increased metabolism and protein synthesis, increased O2 consumption, child growth & development, mental and sexual maturity, increased HR, contractility, cardiac output, increased V, inc. peristalsis, gastric secretion, appetite, inc. skeletal muscle reactivity, SNS stimulation (inc. epi/norepi)
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manifestations of hyperthyroidism
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goiter (compensatory hyperplasia/hypertrophy)
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primary hypothyroidism
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thyroid dysfunction; decreased T3/T4
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secondary hypothyroidism
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anterior pituitary dysfunction (decreased TSH) or hypothalamic dysfunction (decreased TRH)
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etiology of hypothyroidism
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hashimoto's thyroiditis***, iodine deficiency, thyroid cancer treatment (removal, radiation)
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pathophysiology of hypothyroidism
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hypometabolic, myxedema
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manifestations of hypothyroidism
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weak, weight gain w/lost appetite, cold intolerance, dry, rough skin, brittle hair/hair loss, decreased GI motility, lethary, mental dullness
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myxedema
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puffy face, enlarged tongue, hoarse/husky voice, pleural effusion
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myxedematus coma
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life threatening hypothyroidism caused by build-up of unmetabolized drugs (sedatives, analgesics, anesthetics); coma, hypothermia, cardiac collapse, hypoventiliation, metabolic collapse (hyponaturemia, hypoglycemia, lactic acidosis)
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primary hyperthyroidism
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adenoma, multinodal goiter
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secondary hyperthyroidism
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graves disease
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graves disease
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AI disorder, unknown etiology, thyroid stimulated Ab's, hyperthyroidism, goiter, exopthalmus
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cause of grave's exopthalmus
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activations of fibroblasts in orbital tissue behind the eye
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effects of exopthalmus
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risk for corneal ulcerations leading to blindness, extraocular muscle paralysis, involvement of optic nerve
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manifestations of hyperthyroidism
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increased O2 consumption, SOB, hypermetabolism, weight loss w/great appetite, fatigue, muscle cramp, heat intolerance, excessive sweating, excessive SNS activity (nervousness, irritability, tachycardia, palpitations)
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thyroid storm/crisis
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severe thyrotoxicosis
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cause of thyroid storm
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reps. infection, DKA, physical/emotional trauma, surgical manipulation of thyroid
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manifestations of thyroid storm
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sudden onset, very high fever, extreme tachycardia, CHF, angina, agitation, restlessness, delerium
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action of aldosterone
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control of Na, K, H2O balance
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cortisol actions
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metabolism of glucose, protein, and fat; anti-inflammatory, psychic effects, tissue response to humoral and neural influence
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adrogen effects
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secondary sex traits
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Primary adrenal cortical disease/ Addison's disease
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destruction of all layers of the adrenal cortex; despite an increase in ACTH, deficiency in all adrenal cortical hormones
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secondary Addison's insufficiency
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partial destruction of anterior pituitary or hypothalamis; results in chronic metabolic disorder
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etiology of primary adrenal cortical insuffiency
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AI, carcinoma, infection
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manifestations of primary/secondary adrenal cortical insufficiency
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aldosterone & glucocorticoid deficiency, increased ACTH
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effects of aldosterone deficiency
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hyponaturemia, hyperkalemia, ECF deficits, decreased CO, orthostatic hypotension, dehydration, fatigue
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effects of glucocorticoid deficiency
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poor stress tolerance, hypoglycemia, lethargy, GI symptoms (N/V, anorexia, diarrhea)
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effects of increased ACTH
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hyperpigmentation of exposed and unexposed skin
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adrenal crisis
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insufficient adrenal response to stressors,
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etiology of adrenal crisis
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minor illness/injury; abrupt withdrawal of long term supplemental steroids (prednisone)
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patho of adrenal crisis
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inability to increase secretion of adrenal horomones in response to stress
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manifestations of adrenal crisis
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N/V, muscular weakness, severe hypotension, dehydration, vascular collapse
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primary hypercortisolism
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benign/malignant adrenal tumor
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secondary hypercortisolism
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cushing's syndrome; pituitary tumor increases ACTH
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tertiary hypercortisolism
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extrapituitary malignant tumor; secretion of ACTH or CRH; small cell carcinoma of lungs; or long term glucocorticoid therapy "latrogenic cushings syndrome"
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manifestations of cushing's
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exaggerated effects of cortisol, altered fat metabolism, buffalo hump, protruding abdomen, moon face, protein breakdown/muscle wasting, osteoporosis, purple striate
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Diabetes insipidus
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deficiency or decreased response to ADH, "central"/neurologic defect in synthesis of ADH, nephrogenic loss of renal response to ADH
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etiology of diabetes insipidus
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head trauma, surgery near hypothal- tract, genetic disorder affecting V2 receptors in renal tubules, lithium, hyperkalemia, hypercalcemia
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effects of lithium, hyperkalemia, hypercalcemia
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interfere w/action of ADH on collecting tubules
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manifestations of diabetes insipidus
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polyuria, polydypsia, inadequate access to water (hypertonic dehydration, increased serum osmolality)
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SIADH
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failure of negative feedback system or ectopic release
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etiology of SIADH
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cancer (bronchogenic, lymphatic, prostatic, pancreatic), brain tumors, hydrocephalus, head injury
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manifestations of SIADH
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decreased serum osmolality, fluid excess w/dilutional hyponatremia, suppression of RAAS, decreased urine output, decreased hematocrit and BUN (b/c dilution)
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MD
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degeneration of skeletal muscle fibers; combination of hypertrophy, atrophy, and necrosis
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types of MD
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Duchenne's and Becker's
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Duchenne's MD
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most common type of MD; recessive single-gene defect on x-chromosome resulting in defective dystrophin; early onset in males
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Becker's MD
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recessive x-linked defect; common among men w/onset later in life
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patho of DMD
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dystrophin fails to provide normal attachment site for contractile proteins, causing muscle fiber tearing, cell regeneration (initial hypertrophy), proliferation of more defective cells, eventually muscle necrosis and replacement w/adipose and fibrous tissue; death usually in young adulthood
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Age 3-5 DMD
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affected postural hip and shoulder muscles; cannot stand, roll, crawl at correct ages, frequent falling
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Age 7-12 DMD
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imbalance of agonist/antagonist muscles, kyphosculiosis, contractures, joint immobility, wheelchair-bound, cardiomyopathy, common respiratory infections, bowel and bladder control intact
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postural cues of DMD
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walking on toes, stuck out belly, swayed back
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effects of kyphosculiosis in DMD
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decreased depth of resp., hypercapnea, hypoxemia, ineffective cough decreasing clearance of secretions causing infection, respiratory failure
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DMD Dx
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family Hx, physical assessment, increased CK, muscle biopsy, DNA test
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Main complication of DMD
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recurrent respiratory infections
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Main causes of death among DMD
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HF, Resp. failure
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MG
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AI disorder, defective nerve impulse conduction at neuromuscular junction; peak onset around 20-30's, more common among women; peak onset later in life, more common in men
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MG etiology
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presence of Ach receptor Ab, thymus problems (thymoma, thymic hyperplasia)
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Patho of MG
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blockage and eventual destruction of Ach receptor sites, causing weak muscle contraction
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intial s/s of MG
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diplopia, ptosis
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progressive s/s of MG
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fatigue, difficult swallowing, respiratory insufficiency, problems lifting, climbing stairs, speech impairment, dysarthria, increased activity in morning
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Dx of MG
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Hx, physical assessment, nerve stimulation test, Ach receptor IgG present, tensilon test
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nerve stimulation test to Dx MG
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with each stimulating impulse, muscle contraction is weaker and weaker
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Myasthenia crisis
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exacerbated s/s, especially respiratory
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causes of Myasthenia crisis
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stress, pregnancy, alcohol, surgery, emotion
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MG/myasthenic crisis Rx
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quinidine, ATBs, B-adrenergics
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ALS/Lou Gehrig's
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progressive degeneration of motor neuron; onset in mid-adulthood, 50's-60's, common in men, 2-5yr survival after onset
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ALS etiology
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unknown; possible chromosome 21 involvement- deficiency in enzyme getting rid of O2 radicals
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ALS manifestations
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limits in 1 UE, LE muscle cramps, weak, spastic, impaired fine motor skills, fasciculations, atrophy, dysphagia, dysarthria, dysphonia
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complications of ALS
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aspiration; respiratory failure
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Dx of ALS
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EMG, muscle biopsy, physical assessment
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MS
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most common cause of nontraumatic neurologic disability; demyelinating disease of white matter of CNS; usually in young-midaged adults
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most common form of MS
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80% exacerbation/remission
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etiology of MS
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genetic predisposition, N. European descent, precipitating event
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patho of MS
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immune mediated brain, spinal cord, optic nerve injury; CD4, CD8, macrophages invade plaques, injury to oligodendrocytes, demyelination slows/blocks conductions
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Manifestations of MS
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visual field changes, diplopia, abnormal gait, dragging foot, bladder and sexual dysfunction, vertigo, nystagmus, dysarthria, parasthesias, depression, apathy, forgetfulness, inattentiveness
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Clinical courses of MS
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relapse/remit, primary progression, secondary progression, progressive-relapse
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relapse/remit MS
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clear relapse w/complete or partial recovery, no progression, but acute attacks
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primary progression MS
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steady progression w/plateaus or minor improvements
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secondary progression MS
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early relapse/remit, later progression b/c attacks
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progressive-relapsing MS
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steadily progressive, aggravated by acute attacks
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Dx of MS
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MRI (multiple, 3 mos. apart), Hx of 2 or more s/s lasting 24hrs<, increased IgG in CSF, physical assessment
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GB syndrome
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acute inflammatory polyneuropathy causing demyelination of peripheral nerves
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infections precipitating GB
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campylobacter, EB, myco. pneumoniae
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GB prognosis
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80-90% spontaneous recovery
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GB patho
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infiltration of mononuclear cells of dendritic capillaries causing weak limbs, flaccid paralysis
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Manifestations of GB
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ascending paralysis, paresis, rapid progression from LE->UE->resp., tachy/brady-cardia, hyper/hypo-tension, orthostatic hypotension, facial flushing, excessive sweating
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Dx of GB
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Hx of infection, s/s, increased protein in CSF, nerve biopsy
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Parkinson's
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degeneration of basal ganglia, progressive destruction of dopamine producers; genetic, early onset
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cause of primary parkinsons
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idiopathic
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cause of secondary parkinson's
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trauma, infection (encephalitis), drugs (antipsychotics, dopamine blockers), toxins (CO poisoning)
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manifestations of Parkinson's
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tremors*, rigidity*, akinesia/bradykinesia*, postural abnormalities*, pill-rolling, jerking (cogwheel/ratchet-like), problems initiating movement, shuffling, leaning forward, glued to ground feeling, mask-like face, slow monotone speech, dementia
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clical course of parkinson's
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insidious onset, slow s/s progression
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Dx of Parkinson's
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physical assessment, + PET scan
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Alzheimer's
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50-70% of dementia, mid/late adulthood
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patho of alzheimer's
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cortical atrophy, enlarged brain ventricles, neurofibrillary tangles around nerve nucleus, amyloid neuritic plaques
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stage 1 alzheimer's
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2-4 yrs; subtle personality changes, disorientation to time/date, forgetfulness, short-term memory loss
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stage 2 alzheimer's
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years; "confusional state", extreme confusion, decreased insight and verbal skills, wandering/sundowning, impaired judgement, inappropriate social behavior, voracious appetite
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stage 3 alzheimer's
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1-2 yrs; "terminal", unable to recognize family, incontinent, no appetite, seizures, no communication
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Dx of alzheimer's
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by elimination; Hx, physical, CT, MRI
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Spinal cord injuries
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**car crash, violence (knives, guns), falls (elderly), sports injuries
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primary SCI
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compression, ischemia (atherosclerosis), transection, torsion, traction
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secondary SCI
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ischemia (BVinjury), increased IC Ca (hemorrhage, RBC breakdown), inflammation (edema, compression)
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acute complications of SCI
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neurogenic shock, autonomic dysreflexia; 24-72hrs loss of sympathetic innervation- hypotension, bradycardia, hypothermia, flaccid paralysis
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chronic SCI complications
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DVT, PE, atrophy, wounds, UTI
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autonomic dysreflexia
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general sympathetic discharge; return of spinal reflexes around 6 mos. following shock
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etiology of autonomic dysreflexia
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1 or more noxious stimuli
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manifestations of autonomic dysreflexia
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extreme HTN, bradycardia, pounding h/a, stuffy nose, flushed skin/sweating above leasion, pallor/goosebumps below lesion, CVA can occur if untreated
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Incomplete SCI
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central cord syndrome, anterior cord syndrome, brown-sequard syndrome
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central cord syndrome
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mostly in elderly, falls, cervical injury, motor/sensory impairment of arms, shoulders; bowel/bladder impairment
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anterior cord syndrome
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infarction of anterior 2/3's of spinal cord; loss of motor, pain/temp. sensation, intact proprioception, vibration and touch
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brown-sequard syndrome
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damage to 1 side of SC, ipsilateral loss of motor and proprioception, contralateral loss of pain/temp.
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global brain injury
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generalized, hypoxemia, ischemia, cardiac arrest
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focal brain injury
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localized, hemorrhage or clot
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patho of global brain injury
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O2 depletion (10sec.), glucose and glycogen deplection (2-4 min), intracellular ATP depletion (4-5 min), failure of Na/K pump causing cell edema/death, increased glutamate levels
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global BI manifestation
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rostral-caudal progression (front-back), change in LOC, pupillary change
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Diencephalon damage
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lowered LOC (obtunded/nonresponsive), reactive pupils, Normal Doll's eyes response, decorticate posturing, cheyne-stokes respirations
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doll's eyes response
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Norm: when opening eyelids and turning head to side, eyes move in opposite direction of head movement
Abnormal: eyes remain centered when moving head side to side |
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decorticate posturing
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arms are folded in toward the chest w/fists
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global BI-midbrain
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comatose, abnormal doll's eyes, nonreactive pupils, neuro. hyperventilation, decerebrate posturing
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decerebrate posture
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arching of back and head, extended legs and arms, outward flexion of arms/wrists
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global BI-pons
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absent corneal reflex, dysconjugate gaze (drifting eyes), irregular respiration
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global BI- medulla
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loss of cough and gag reflexes, apnea, flaccidity
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etiology of focal BI
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trauma, tumor, stroke, hematoma, edema, IICP, ischemia
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concussion
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mild head injury causing momentary loss of consciousness and possible amnesia
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post concussion syndrome
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vague, persistent, h/a, irritation, insomnia, poor concentration/memory, subtle personality change
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epidural hematoma
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b/t brain and skull- arterial bleed; rapid onset, brief lucidity and unconsciousness, lower LOC, ipsilateral pupil dilation, contralateral hemiparesis
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subdural hematoma
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b/t dura and arachnoid- venous bleed; catagorized as acute, subacute, or chronic
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acute subdural bleed
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24-48 hrs neurological deficits after injury
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subacute subdural bleed
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48-2wks post injury; loss of consciousness over hrs, eventually nonresponsive
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chronic subdural bleed
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very slow, over months to yrs postinjury, common in elderly and alcoholics
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manifestations of chronic subdural bleed
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nonspecific, h/a, apathy, lethargy, decreased attention, loss of higher cognitive skills
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cerebral edema
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increased ECF
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patho of cerebral edema
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leakage of plasma proteins and H2O from capillaries
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CPP
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pressure required to perfuse brain tissue
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normal CPP
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70-100 mmHg
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ischemic CPP
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<50-70 mmHg
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CPP equation
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CPP=MAP - ICP
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IICP
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>15 mmHg; failure of or overwhelmed autoregulation of ICP, as ICP increasing, CPP decreases
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etiology of IICP
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trauma, tumor, edema, bleeding, increased CSF, head injury
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early s/s IICP
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peripheral vasoconstriction causes lower LOC, transient confusion/drowsiness
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progression of s/s IICP
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systemic arterial HTN, h/a, papilledema, projectile vomiting, sluggish dilation of pupils, decorticate posture, cheyne-stokes respiration, cushing's triad
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cushing's triad
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severe HTN (inc. S/dec. D), widened pulse pressure, bradycardia
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brain death
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when ICP=SBP, cerebral blood flow stops
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types of skull Fx
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linear, depressed, basilar
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basilar skull Fx
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ethmoid cribiform, CSF leakage- otorrhea or rhinorrhea, ecchymosis behind ears, raccoon eyes
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brain attack
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aka CVA or stroke; acute focal neurologic defecit r/t a vascular disorder
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risks for CVA
|
old age, gender (male), AA, HTN, smoking, high cholesterol, Afib, polycythemia, sickle cell anemia, atherosclerosis
|
|
|
thrombotic stroke
|
atherosclerotic plaques typically at arterial bifurcations
|
|
|
site of origin for embolic stroke
|
L heart, carotid arteries, aortic arch
|
|
|
predisposing conditions for embolic stroke
|
Afib, MI, ventricular aneurysm, rheumatic heart disease
|
|
|
TIA
|
"warning sign"/"mini-stroke", area of penumbra w/o necrotic core, s/s resolve in 24 hrs
|
|
|
R brain damage manifestations
|
L-sided paralysis "hemiplegia", L-side neglect, spatial perception difficulty, minimize problems, impulsive, short attention span, impaired concept of time, impaired judgement
|
|
|
L brain damage manifestations
|
depression, anxiety, awareness of deficits, R sided paralysis, aphasia, cautious
|
|
|
patho of seizures
|
alteration in cell membrane permeability and ion distribution, excess Ach, decreased GABA
|
|
|
etiology of provoked seizures
|
hyperthermia (<5yo), metabolic disturbance (alkalosis, hypoxia, hypoglycemia), drugs (cocaine, withdrawal), brain lesions
|
|
|
manifestations of seizure
|
recall of past events, olfactory hallucinations, repetitive motion, absence of motion
|
|
|
partial seizure
|
activity begins in localized area of one hemisphere
|
|
|
generalized seizure
|
simultaneous onset of seizure activity in both hemispheres of cerebral cortex
|
|
|
jacksonian epilepsy
|
epilepsy w/simple partial seizures with sequential involvement of body parts
|
|
|
simple partial seizure
|
unilateral twitching/tingling, conscious- jacksonian epilepsy
|
|
|
complex partial seizures
|
conscious behavior but amnesic, may be provoked, repetitive movement, inappropriate behavior
|
|
|
types of generalized seizures
|
absence, tonic-clonic
|
|
|
absence seizures
|
brief LOC, usually in kids
|
|
|
tonic-clonic seizures
|
preceeded by an aura, tonic muscle tension, clonic muscle jerking, incontinence of bowel and bladder, postictal period
|
|
|
infections of the CNS
|
meningitis, encephalitis, myelitis, encephalomyelitis
|
|
|
meningitis
|
inflammation of pia mater, arachnoid and subarachnoid space; chemical, bacteria, or viral
|
|
|
acute pyogenic meningitis
|
bacteria meningitis
|
|
|
acute lymphocytic meningitis
|
viral meningitis
|
|
|
bacterial meningitis- types
|
most common- strep.pneumoniae, h. influenzae, n. meningitidis
|
|
|
risks for bacterial meningitis
|
very young, very old, immunocompromised, head trauma, otitis, sinusitis, neurosurgery
|
|
|
patho of meningitis
|
bacteria replicate and lyse in CSF, release endotoxins, inflammatory mediators emigrate, CSF congestion, meninges thicken
|
|
|
manifestations of meningitis
|
fever, chills, h/a, stiff neck, abdominal pain, N/V, petechiae (meningococcal)
|
|
|
Dx of meningitis
|
Hx, physical, lumbar puncture, cloudy CSF
|
|
|
lab values for CSF w/meningitis
|
increased neutrophils (>90,000), protein, decreased glucose, visible bacteria on smear
|
|
|
Tx of meningitis
|
antibiotics, corticosteroids, vaccines
|
|
|
viral meningitis
|
similar to bacterial, but less severe, self-limiting
|
|
|
CSF lab values for viral meningitis
|
increase lymphocytes, protein only moderately elevated, normal glucose content
|
|
|
encephalitis
|
generalized infection of spinal cord or brain, usually viral but can be bacterial, bite or ingestion transmission, most common in US is HSV (herpes simplex virus)
|
|
|
patho of encephalitis
|
local necrotizing hemorrhages, become generalized, result in prominent edema, progressive degeneration of nerve cell bodies
|
|
|
manifestations of encephalitis
|
fever, h/a, neck stiffness, seizure, confusion, coma
|
|
|
Dx of encephalitis
|
Hx, s/s, spinal tap, CSF analysis
|
|
|
etiology of malabsorption
|
gastric surgery, pancreatic disorder, hepatobiliary disorder, lumen disease
|
|
|
manifestations of malabsorption
|
weight loss, diarrhea, steatorrhea, flatulence, bloating, abdominal pain, abdominal distention
|
|
|
IBS; etiology
|
unknown, thought to be caused by emotion or hormones (menstruation)
|
|
|
path of IBS
|
dysregulation of intestinal sensory and motor function modulated by CNS
|
|
|
3 mo.s of IBS manifestations
|
abdominal pain relieved by defecation,change in freq. or consistency of stool, change in pattern of defecation
|
|
|
IBD
|
crohns and colitis
|
|
|
etiology of IBD
|
unknown, possible infection by chlamydia or mycobacterium, AI, genetic predisposition
|
|
|
Crohn's
|
recurrent granulomatous lesions of small and large intestines
|
|
|
granulomas
|
growths resulting from engulfment of foreign bodies and bacteria by macrophages
|
|
|
etiology of Crohn's
|
unknown, higher occurence in europeans and ashkenazi jews, onset in adolescence or young adulthood
|
|
|
patho of crohn's
|
inflammation of intestinal submucosa moving into the mucosa and serosa, cobblestone fissures "skip pattern"
|
|
|
manifestations of crohn's
|
exacerbations/remission, intermittent diarrhea (possibly bloody), abdominal tenderness, RUQ pain, malaise, low grade fever, malabsorption (weight loss, anemia, hypoalbuminemia, steatorrhea)
|
|
|
complications of crohn's
|
fistulas, abscesses
|
|
|
colitis
|
inflammatory condition of the mucosal layer of colon and rectum; can have 30-40 BMs/day with bloody and mucus stools
|
|
|
etiology of colitis
|
unknown, AI, increased colon Ab's, in young adults
|
|
|
etiology of malabsorption
|
gastric surgery, pancreatic disorder, hepatobiliary disorder, lumen disease
|
|
|
manifestations of malabsorption
|
weight loss, diarrhea, steatorrhea, flatulence
|
|
|
IBS; etiology
|
unknown, thought to be caused by emotion or hormones (menstruation)
|
|
|
path of IBS
|
dysregulation of intestinal sensory and motor function modulated by CNS
|
|
|
3 mo.s of IBS manifestations
|
abdominal pain relieved by defecation,change in freq. or consistency of stool, change in pattern of defecation
|
|
|
IBD
|
crohns and colitis
|
|
|
etiology of IBD
|
unknown, possible infection by chlamydia or mycobacterium, AI, genetic predisposition
|
|
|
Crohn's
|
recurrent granulomatous lesions of small and large intestines
|
|
|
granulomas
|
growths resulting from engulfment of foreign bodies and bacteria by macrophages
|
|
|
etiology of Crohn's
|
unknown, higher occurence in europeans and ashkenazi jews, onset in adolescence or young adulthood
|
|
|
patho of crohn's
|
inflammation of intestinal submucosa moving into the mucosa and serosa, cobblestone fissures "skip pattern"
|
|
|
manifestations of crohn's
|
exacerbations/remission, intermittent diarrhea (possibly bloody), abdominal tenderness, RUQ pain, malaise, low grade fever, malabsorption (weight loss, anemia, hypoalbuminemia, steatorrhea)
|
|
|
complications of crohn's
|
fistulas, abscesses
|
|
|
colitis
|
inflammatory condition of the mucosal layer of colon and rectum, continuous throughout, begins at rectum and ascends through colon
|
|
|
etiology of colitis
|
unknown, AI, increased colon Ab's, in young adults
|
|
|
patho of colitis
|
inflammation of lieberkuhn secretory glands, inflammation of crypts causes pinpoint mucosal hemorrhages, abscess, ulceration and necrosis
|
|
|
manifestations of colitis
|
remission/exacerbation, abdominal pain, diarrhea, rectal bleeding, anorexia, fatigue
|
|
|
risks w/colitis
|
increased risk for colon cancer (20-30 x's general population)
|
|
|
infectious colitis
|
inflammation and infection of colon
|
|
|
two common causes of infectious colitis
|
c. diff., e.coli
|
|
|
hepatitis
|
inflammation of the liver
|
|
|
etiology of hepatitis
|
drugs, toxins, microorganisms, AI
|
|
|
viral hepatitis etiology
|
50% Hep A RNA virus, Hep B DNA virus, Hep C, D, E
|
|
|
patho of viral hepatitis
|
direct hepatocellular injury d/t immune response, necrosis
|
|
|
phases of hepatitis
|
prodromal/preicterus, icterus, convalescence/recovery
|
|
|
prodromal/preicterus phase of hepatitis
|
RUQ pain, circulating immune complexes (malaise, low grade fever, arthralgia, rash), anorexia, weight loss, fatigue
|
|
|
lab values for prodromal hepatitis phase
|
elevated AST/ALT
|
|
|
normal AST level
|
5-35
|
|
|
normal ALT level
|
5-35
|
|
|
normal ALP level
|
30-120
|
|
|
icteric phase of hepatitis
|
jaundice, rise in serum bilirubin, dark urine, pale stool, hepatosplenomegaly, tender lymphadenopathy, prolonged PTT
|
|
|
norm indirect bilirubin level
|
0.2-0.7; unconjugated
|
|
|
norm direct bilirubin level
|
0.1-0.3; conjugated
|
|
|
norm total bilirubin
|
0.3-1.0; direct + indirect
|
|
|
convalescent/recovery phase of hepatitis
|
easily fatigued, normal liver function tests in 3-6 mo.
|
|
|
cirrhosis
|
replacement of normal liver cells with fibrous tissue
|
|
|
types of liver dysfunction
|
hepatocellular dysfunction, portal HTN, ascites, hepatic encephalopathy
|
|
|
endocrine disturbances- estrogen
|
gynomastia, testicular atrophy, amennhorea, spider angiomas, pectoral and axillary alopecia, palmer erythema
|
|
|
hematologic disturbances
|
clotting factors, splenomegaly, folate/B12/iron deficiencies
|
|
|
portal HTN
|
increased resistance to blood flow in portal system by obstruction or constriction; ascites
|
|
|
ascites
|
accumulation of fluid in intraparitoneal space
|
|
|
manifestations of ascites
|
increase in abdominal girth, + fluid wave, tenderness, SOB
|
|
|
hepatic encephalpathy
|
cerebral intoxification d/t decreased NH3 metabolism; progressive decrease in neurological functioning
|
|
|
manifestations of hepatic encephalpathy
|
subtle personality/behavioral changes, vacant stare, slurred speech, inappropriate responses, disrespectful, uncooperative, change in sleep patterns, loss of sphincter control, asterixis "liver flap", apraxia, confusion, hyperventiliation, hypothermia, hyperactive reflex, + babinski
|
|
|
acute pancreatitis
|
inflammation of acinar/exocrine pancreas
|
|
|
etiology of pancreatitis
|
alcoholism, biliary obstruction
|
|
|
patho of pancreatitis
|
reflux of bile or duodenal contents activates digestion enzymes (phospholipase A, elastase, kallikrein)
|
|
|
manifestations of pancreatitis
|
severe abdominal pain radiating to the back, N/V, hypo/hyper-active bowel sounds, diaphoresis, bruising around umbilicus/flanks (grey turner's sign, cullen's sign), fever, tachycardia, hypotension
|
|
|
lab changes in pancreatitis
|
serum amylase 60-180, urine amylase 35-360, lipase <1.5, WBC>10000, hyperglycemia, hypocalcemia
|
|
|
complications of pancreatitis
|
DM, chronic pancreatitis, tetany, pleural effusion, abscesses, peritonitis
|
|
|
chronic pancreatitis
|
chronic inflammation leading to fibrosis and calcification
|
|
|
etiology of chronic pancreatitis
|
75% chronic alcoholism; free radicals, acetaldehye
|
|
|
manifestations of chronic pancreatitis
|
steatorrhea, weight loss, hyperglycemia, malabsorption, malnutrition, DM
|
|
|
solubility of direct bilirubin/conjugated
|
water soluble
|
|
|
solubility of indirect bilirubin/unconjugated
|
fat soluble; must be transported to liver by plasma proteins
|
|
|
intraluminal maldigestion
|
defect in processing nutrients in intestinal lumen
|
|
|
causes for intraluminal maldigestion
|
pancreatic insufficiency, hepatobiliary disease, intraluminary bacterial growth
|
|
|
transepithelial transport maldigestion
|
mucosal lesions impair uptake across mucosal surface
|
|
|
causes of transepithelial transport maldigestion
|
celiac disease, crohn's disease
|
|
|
lymphatic obstruction maldigestion
|
interference with transport of products of fat digestion into systemic circulation
|
|
|
causes of lymphatic obstruction maldigestion
|
congenital, neoplasms, trauma, infectious disease
|
|
|
manifestations of vitamin K deficiency
|
easy bleeding and bruising, bone pain, risk for Fx, tetany
|
|
|
complications/results of malabsorption
|
macrocytic anemia, glossitis (folic acid def.), neuropathy, skin atrophy, edema
|
|
|
prevalence of IBS
|
10-20% people in Western countries
|
|
|
Dx of IBS
|
12 weeks of s/s
|
|
|
similarities in IBD's (crohn's and colitis)
|
inflammation of bowel, no known etiology, familial, systemic manifestations
|
|
|
systemic manifestations of IBD
|
spinal/joint arthritis, eye inflammation/uveitis, skin lesions, stomatitis, AI anemia, hypercoagulability
|
|
|
areas effected by Crohn's
|
30% small bowel, 30% large bowel, 40% combo
|
|
|
prevalence of crohn's
|
more common in women than men
|
|
|
types of colitis
|
mild chronic, chronic intermittent, acute fulminatin
|
|
|
mild chronic colitis
|
most common; minimal systemic s/s, mild bleeding and diarrhea
|
|
|
chronic intermittent colitis
|
more colon surface effected, more systemic s/s
|
|
|
acute fulminating colitis
|
15% prevalence; entire colon involved, severe, bloody diarrhea, fever, abdominal pain, risk for toxic megacolon
|
|
|
C. diff
|
spore-forming bacillus often resulting from use of broad-spectrum antibiotic for unknown infection
|
|
|
risks for C. diff
|
hospitalization, health care workers
|
|
|
manifestations of C.diff
|
profuse diarrhea, lower abdominal pain
|
|
|
complication of C.diff
|
P.colitis
|
|
|
P. colitis
|
false membrane formation over an area of inflammation
|
|
|
manifestations of P.colitis
|
acute illness s/s: lethargy, tachycardia, abdominal pain, distention, risk for toxic megacolon
|
|
|
toxic megacolon
|
loss of smooth muscle tone, risk for perforation of intestine
|
|
|
e. coli
|
"hamburger disease", food borne bacteria by undercooked food
|
|
|
complications of e.coli
|
toxemia, hemolytic-urenic syndrome, thrombotic thrombocytopenia purpura
|
|
|
hemolytic-urenic syndrome
|
hemolytic anemia, thrombocytopenia, and renal failure; 5-10% mortality rate, 30% permanently disabled
|
|
|
diverticulosis
|
herniated mucosa through muscular colon wall- formation of diverticula
|
|
|
cause of diverticulosis
|
unknown, possibly low roughage diet
|
|
|
manifestations of diverticulosis
|
often asymptomatic, mild flatus, diarrhea alternating w/constipation
|
|
|
diverticulitis
|
inflammation of diverticula
|
|
|
manifestations of diverticulitis
|
LLUQ pain/tenderness, N/V, minor bleeding, risk for abscess (rupture, perforation, peritonitis)
|
|
|
manifestions of bowel abscess
|
fever, leukocytosis, LLQ tenderness
|
|
|
manifestations of bowel perforations
|
LLQ pain, rigidity
|
|
|
etiology of intestinal obstruction
|
paralytic ileus, mechanical obstruction
|
|
|
paralytic ileus
|
inhibition of peristalsis d/t abdominal surgery, anesthesia, or immobility
|
|
|
mechanical obstruction
|
tissue adhesion r/t prior surgery, tumor, volvalus, intussusception (children)
|
|
|
manifestations of paralytic ileus
|
hypoactive bowel sounds, abdominal distention, cramping, pain, vomiting, constipation
|
|
|
manifestations of mechanical obstruction
|
hyperactive bowel sounds at first, followed by absence of bowel sounds; abdominal distention, cramping, pain, vomiting, constipation
|
|
|
polyps
|
growths on mucosal surface
|
|
|
tubular pedunculated adenomas
|
<2cm globelike tumors attached by stalks
|
|
|
complication for tubular pedunculated adenomas
|
increased risk for colon cancer w/increasing size of tumors >1cm
|
|
|
villous adenomas
|
broad-based nodular tumors; less common than pedunculated; found in sigmoid colon or rectum, 25% become cancerous
|
|
|
tubulovillous
|
combination of tubular and villous adenomas, risks run in between the two, risk for obstruction
|
|
|
colon cancer
|
2nd leading cancer death in US; adenocarcinoma of large intestine
|
|
|
etiology of colon cancer
|
low roughage diet, high fat diet, diet high in refined carbs, 50-60 y/o
|
|
|
risks leading to colon cancer
|
ulcerative colitis, familial polyposis
|
|
|
familial polyposis
|
rare autosomal dominant trait resulting in many pedunculated and villous adenomas that turn cancerous by 40 y/o
|
|
|
manifestations of colon cancer
|
change in bowel habits, rectal bleeding, pain, anemia
|
|
|
markers for cecum/ascending colon cancer
|
guiac + stools, anemia
|
|
|
markers of rectal/sigmoid colon cancer
|
diarrhea, blood mucus stool, distention, anemia, obstruction, narrow ribbony stool
|
|
|
colon cancer metastasis pathways
|
direct infiltration (bladder), lymphatic spread, portal vein access to liver
|
|
|
pyelonephritis
|
upper urinary tract infection
|
|
|
effects of pyelonephritis
|
more systemic effects vs. lower UTI b/c closer to vascular system
|
|
|
acute pyelonephritis risks (6)
|
untreated low UTIs, pregnancy, immunosuppressed, women (b/c high risk for low UTI), neurogenic bladder (SCI, DM), vesicoureteral reflux/VUR
|
|
|
VUR
|
congenitally short portion of ureter in bladder wall, causing reflux into kidneys and bladder
|
|
|
risks for chronic pyelonephritis (2)
|
urinary obstruction, VUR
|
|
|
patho of pyelonephritis
|
inflammation, destruction of nephron basement membrane, tubule dysfunction, polyuria & dilute urine
|
|
|
manifestations of acute pyelonephritis
|
very high abrupt fever, chills, constant back pain, C/V tenderness, leukocytosis (>10,000), pyuria, bacteriuria, nitrites in urine, leukocytestherase in urine
|
|
|
manifestations of chronic pyelonephritis
|
vague, polyuria, nocturia, low grade fever (less bacteria, WBCs b/c antibiotics)
|
|
|
glomerulonephritis
|
inflammation of kidneys beginning in glomerulus, leading to ESRD
|
|
|
patho of glomerular disease
|
injury to glomerulus d/t Ab/Ag complex deposits (Type 3 hypersensitivity rxn)
|
|
|
Acute proliferating glomerulonephritis etiologies (4)
|
STREP. A, chicken pox, mumps, measles
|
|
|
onset of acute glomerulonephritis
|
7-12 days to manifest b/c Ab production; s/s resolve in 10-14 days w/possible residual proteinuria
|
|
|
patho of acute glomerulonephritis
|
strep A begins Ag/Ab rxn, deposits in glomerular basement membrane, swelling of glomerular capsule, increased porosity in membrane to proteins and RBCs, inc. porosity decreases GFR, release aldosterone, RAAS activation (vasoconstriction), Na/H2O retention, EDEMA & HTN
|
|
|
manifestations of glomerulonephritis
|
proteinuria, hematouria, edema, HTN, azotemia, cola-colored urine, oliguria (<400 mL/day)
|
|
|
rapid progressive glomerulonephritis
|
severe injury to glomerulus causes decline in 2-3 mos., eventual progression to chronic renal failure
|
|
|
etiology of rapid progressive glomerulonephritis (2)
|
SLE, goodpasture's
|
|
|
goodpasture's
|
Ab directly fight against glomerular basement membrane; eventual lung involvement and pulmonary infection
|
|
|
norm GFR
|
110-130
|
|
|
primary etiology of chronic glomerulonephritis
|
renal disease
|
|
|
secondary etiologies of chronic glomerulonephritis (4)
|
SLE, amyloidosis, DM, HTN
|
|
|
manifestations of nephrotic syndrome
|
50% of those w/glomerulonephritis; massive proteinuria (>3.5/day), hypoalbuminemia, edema, hyperlipidemia
|
|
|
complications of chronic glomerulonephritis (3)
|
vulnerability to infection (b/c low protein availability/globulin loss), thrombosis, pulmonary edema
|
|
|
types of acute RF (3)
|
prerenal, postrenal, intrinsic/intrarenal
|
|
|
effects of acute RF
|
rapid onset, inc/dec. output, 40-70% mortality, fluid/electrolyte imbalance, pH change
|
|
|
azotemia
|
increased BUN (>18), increased uric acid, increased creatinine
|
|
|
best marker for RF
|
creatinine
|
|
|
etiology of acute RF- prerenal
|
decreased renal perfusion d/t: decreased CO, fluid volume deficit, ineffective circulation
|
|
|
acute RF- prerenal
|
most common form of reversible RF
|
|
|
normal renal CO
|
20-25%
|
|
|
norm Creatinine:BUN
|
10:1
|
|
|
prerenal acute RF C:BUN
|
15-20:1
|
|
|
high risk for fluid volume deficit
|
burn, excessive V/D, anterior wall MI, severe dehydration, anaphylactic/septic shock, GI bleed
|
|
|
occurence of acute prerenal RF
|
55-60%
|
|
|
occurence of acute postrenal RF
|
<5%
|
|
|
occurence of acute intrinsic/intrarenal RF
|
35-40%
|
|
|
etiologies of acute postrenal RF (4)
|
stones/caliculi, BPH (men), ureteral stricture, tumor
|
|
|
etiologies of acute intrarenal RF (3)
|
ATN, strep. glomerulonephritis, malignant HTN
|
|
|
ATN
|
necrosis of tubular epithelium leading to necrosis of basement membrane
|
|
|
etiologies of ATN (2)
|
nephrotoxic drugs, ischemic event (hypoxia, hypoperfusion)
|
|
|
nephrotoxic drugs
|
antibiotics, contrast media, heavy metals, solvents
|
|
|
phases of acute RF (3)
|
onset, maintenence, recovery
|
|
|
onset phase of acute RF
|
hrs-days; precipitating event leads to injury
|
|
|
maintenence phase of acute RF
|
sudden oliguria (<400/day), change in specific gravity, casts in urine, retention of metabolic waste (urea, creatinine, hypernatremia, hyperkalemia), edema
|
|
|
recovery phase of acute RF
|
output >400/day, decrease in azotemia, restore norm BUN/creatinine
|
|
|
risks for chronic RF
|
HTN, DM, PKD, glomerulonephritis
|
|
|
phases of chronic RF (4)
|
decreased renal reserve, renal insufficiency, renal failure, ESRF/ESRD
|
|
|
decreased renal reserve phase of chronic RF
|
gradual decline in GFR, norm BUN/creatinine, norm output
|
|
|
renal insufficiency phase of chronic RF
|
50-80% loss in nephrons, mild azotemia, rising creatinine, nocturia, polyuria, HTN
|
|
|
usual excretion of potassium
|
80%
|
|
|
renal failure phase of chronic RF
|
80-90% loss in nephrons, edema, metabolic acidosis, hyperkalemia
|
|
|
uremic syndrome
|
systemic effects from accumulation of nitrogenous wastes
|
|
|
manifestations of uremic syndrome
|
metabolic acidosis ->kussmaul's resp., hyperkalemia, hypernatremia, hyperuricemia, hypocalcemia, hyperphosphatemia, anemia, etc.
|
|
|
EKG effects of hyperkalemia
|
long PRI, wide QRS, peaked T
|
|
|
effects of hypernatremia
|
edema, CHF, HTN
|
|
|
effects of hyperuricemia
|
salt deposits in soft tissue & joints-> gouty arthritis
|
|
|
patho of uremic syndrome hypocalcemia
|
increased PTH, bone reasborption, risk for Fx, precipitation of salts in joints, skin
|
|
|
patho of hyperphosphatemia in uremic syndrome
|
decreased vit D production, less Ca absorption, hypocalcemia, lower GFR, less PO4 retention
|
|
|
patho of uremic syndrome anemia
|
lower RBC lifespan, bleeding tendencies b/c platelet defects, Fe/Folic acid deficiency, less RBC prod. b/c less/inactive erythropoietin or suppressed marrow
|
|
|
sexual effects of uremic syndrome
|
W: menstrual cessation, hypofertility
M: impotence, lowered lobido |
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cardiovascular effects of uremic syndrome
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HTN, CHF
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respiratory effects of uremic syndrome
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pulmonary edema, pneumonitis, dyspnea
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immune effects of uremic syndrome
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increased infection rate d/t lower protein levels, delayed hypersensitivity, poor nutrition, direct vascular access (dialysis pts)
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skin effects of uremic syndrome
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urochrome pigments (yellow/waxy, yellow/brown, ashen/gray), pruritis (PO4 deposits), uremic frost
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GI effects of uremic syndrome
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N/V
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metabolic effects of uremic syndrome
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insulin resistence, inc. triglycerides, inc. cholesterol
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neuromuscular effects of uremic syndrome
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irritable, peripheral neuropathy
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progression of neuropathy r/t uremic syndrome
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slow nerve conduction -> sensory changes in toes/feet -> motor involvement (foot drop, paralysis)
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