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Final Concept Review I.

GU Disorders: See Week 5 Check in! A. Acute renal failure: is reversible! 1. Determining prognosis: if they respond to the diuretic with good urine output, then they are functioning fine! 2. This is a sudden decline in kidney function with a decrease in glomerular filtration and urine output with an accumulation of nitrogenous waste products in the blood as demonstrated by an elevation in plasma creatinine and BUN levels. ! 3. Pre-renal: most common cause and is due to inadequate kidney perfusion. This can be due to hypotension, hypovolemia, sepsis, inadequate cardiac output, multiple organ dysfunction, renal vasoconstriction, renal artery stenosis, or kidney edema. ! 4. Intra-renal: usually due to ischemic acute tubular necrosis, nephrotoxic ATN (contrast or ABX), acute glomerulonephritis, vascular disease, allograft rejection, or interstitial disease! 5. Post-renal: occurs with a urinary tract obstruction that affects the kidneys bilaterally. There is an increase in intraluminal pressure upstream from the site of the obstruction with a gradual decrease in GFR. ! 6. Clinical Manifestations include:

Table 39.11 Urine Characteristics of Prerenal and Intrinsic Acute Kidney Injury Diagnostic Index

Prerenal

ATN

Urine Volume

6.5%!

5 2. Endocrine actions of insulin: insulin promotes glucose uptake in the liver, muscle, and adipose tissue! 3. A common complication of Type 2 is autonomic neuropathy! a) This includes GI symptoms: decrease esophageal motility, gastroparesis, and decreased gastric emptying! 4. Hypoglycemia can occur! a) This manifests as increase heart rate, palpitations, diaphoresis, tremors, pallor, and arousal anxiety! b) Reverse with sugars ASAP!! F. Hyperparathyroidism: Stimulation of the parathyroid gland in response to hypocalcemia! 1. Hypercalcemia and hypophosphatemia: asymptomatic or related to neuromuscular changes that include paresthesia and muscle cramps! a) Decreased calcium have low bone density that is noted in the distal 1/3 radius. This is common in the elderly population. ! G. Hypoparathyroidism! 1. This is characterized by abnormally low PTH levels usually due to damage or removal of the parathyroid glands. ! 2. It is caused by a lack of circulating PTH which causes serum calcium levels to decrease and serum phosphate levels to increase. ! 3. The hypomagnesemia inhibits the action of PTH! 4. May be related to chronic alcoholism, malnutrition, malabsorption, increased renal clearance of magnesium due to an amino glycoside, or prolonged magnesiumdeficient parenteral nutrition.! 5. Hypocalcemia manifests as: dry skin, loss of body and scalp hair, hypoplasia of developing teeth, horizontal ridges, cataract, basal ganglia, calcification, deformities, bowing of the long bones! 6. Treatment is focused on correcting the low calcium ! H. Hypercortisolism! 1. Glucose intolerance because of cortisol-induced insulin resistance and increase gluconeogenesis and glycogen storage by the liver! 2. Cushing’s Syndrome manifests as: fat deposition, truncal obesity, moon face, buffalo hump! I. Hypocortisolism: Adrenal Crisis! 1. Onset typically manifests as hypotension! 2. Can progress to complete vascular collapse and shock! 3. Known as adrenal/Addisonian crisis! 4. Typically develops with undiagnosed disease, acute withdrawal of glucocorticoids, or occurrence of infection/stressful event! 5. Primary hypocortisolism! a) Labs show serum and urine levels of cortisol are depressed and increased ACTH! b) When prescribing cortisol, the NP should remember: acute stressors may indicated a need to increase the comparable natural levels! V. Neurodegenerative Diseases! A. Alzheimer’s: decreased short-term memory occurs with mild cognitive decline due to decreased hippocampus size! 1. Greatest risk factors are: age and family history! 2. Exact cause is unknown, but thought to be related to the amyloid beta complexes! 3. Clinical Manifestations include: forgetfulness, problem solving difficulties, etc! 4. Treatment is aimed at helping with memory aid! B. Parkinson’s! 1. The hallmark pathologic features of PD are loss of dopaminergic pigmented neurons in the substantial nigra and dopamine loss in other brain areas. !

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C.

D. E.

F. G. H.

I.

2. Clinical Manifestations include: Bradykinesia and shuffling gait, resting tremor, rigidity, postural disturbance, dysarthria, dysphagia! Demyelinating Disease: MS! 1. MS is a chronic inflammatory disease involving the degeneration of CNS myelin, scarring, and loss of axons! 2. The loss of myelin disrupts nerve conduction which causes symptoms! 3. Risk factors: smoking, vitamin D deficiency, Epstein-Barr Virus! 4. Clinical Manifestations include; paresthesias, weakness, impaired gait, visual disturbances, urinary incontinence! Febrile Seizures: one possibility is that neurons are excited by decreased carbon dioxide levels due to hyperventilation in febrile state! 1. Increased body metabolism! Headache Syndromes: Review in general! 1. Cluster Headache: characterized by unilateral trigeminal distribution of severe pain with ipsilateral autonomic manifestations like tearing on affected side, ptosis, and congestion of nasal mucosa! a) Pain may alternate sides with each episode, is usually severe, stabbing and throbbing, and referred to mid face and teeth! 2. Migraine: episodic neuordIsorder whose marker is a headache lasting 4-72hrs, diagnosed by 2 or more of these symptoms: unilateral pain, throbbing pain, pain that worsens with activity, moderate-severe pain intensity, nausea/vomiting, photophobia, and photophobia! a) Aura with visual, sensory or motor symptoms, without aura, or chronic! 3. Tension: most prevalent, no vascular or migrainous, onset usually in the 2nd decade, mild-moderate bilateral headache with sensation of tight band or pressure around the head! Bell’s Palsy: Cranial Nerve 7! 1. Characterized by facial asymmetry and inability to close eye, smile, or frown on affected side.! Trigeminal neuralgia: is associated with compression of cranial nerve 5! 1. Results in severe and sharp stabbing pain that worsens with chewing ! Bacterial Meningitis! 1. Clinical Manifestations include: fever, increased heart rate, chills, meningeal irritation, severe throbbing Headache, severe photophobia, nuchal rigidity, and positive Kernig and Brudzinski signs! Cerebrovascular Accident! 1. Review signs and symptoms depending on artery infarcted!

Stroke Symptoms Location/Vessel

Signs and Symptoms Noted

Basilar Artery

Motor: contralateral hemiparesis or hemiplegia, ipsilateral lower motor neuron facial palsy! Sensory: contralateral loss of vibratory sense, sense of position with dysmetria, loss of two-point discrimination, impaired rapid alternating movements ! Visual: inferior pontine: diplopia; impaired abduction of ipsilateral eye; internuclear ophthalmoplegia; medial superior; diplopia, internuclear

7 Stroke Symptoms Posterior cerebral artery

Motor: contralateral hemiplegia with possible dysmetria, dyskinesia, hemiballism, choreoathetosis, dystaxia, cerebellar ataxia, and tremor! Sensory: contralateral sensory loss of all modalities without agraphia! Function: prosopagnosia, topographic disorientation, memory deficits, Alexia, inability to read colors

2. Infarct in AVA causes motor problems! 3. Sensory deficits associated with basilar artery infarct include contralateral loss of vibratory sense, sense of position with dysmetria, loss of two point discrimination, impaired rapid alternating movements! VI. Dermatological! A. Rosacea: familial tendency and several genes have been identified! 1. Neurovascular dysregulation, infection, and factors that trigger altered innate and adaptive immune responses are involved! B. Melanoma: most aggressive skin cancer! 1. The thickness of the lesion impacts the prognosis! C. Plaque Psoriasis: well-demarcated, thick, silvery, sadly, erythematous plaque surrounded by normal skin...