4 star topics Flashcards
Most common causes of acute pericarditis
Viral infections - HIV Bacterial - TB especially Neoplasms - mets or primary Trauma (CPR, cardiac surgery) Complications of MI (Dressler's Sn 2-4 weeks post MI) Rheumatologic disease (SLE, RA) Renal failure - uremic pericarditis Radiation Drugs
Clinical findings suggestive of acute pericarditis
Pleuritic CP - worse with coughing or inspiration; worse when supine; better when sitting up and leaning forward
PE: pericardial friction rub
Testing:
ECG - diffuse ST elevation, PR depression
ECHO: pericardial effusion - usually transudative; exudative - neoplasm, TB; absent does not r/o
CXR: usually nl, may show enlarged cardiac silhouette - canteen heart
Treatment of acute pericarditis
NSAIDs - ibuprofen, indomethacin
Colchicine
If no response in 1-2 weeks, look for other cause - neoplasm, bacterial, SLE, recent MI
Causes of cardiac tamponade
pericarditis
hemorrhage - chest trauma, aortic dissection
Physical exam findings suggest cardiac tamponade
Beck’s triad: hypotension, JVD, muffled heart sounds
Pulsus paradoxus - decreased capacity of LV
-SBP decreases >10 mmHg with inspiration
Diagnostic tests in cardiac tamponade
ECHO - pericardial effusion/fluid, collapse of ventricles
ECG: low voltage, electrical alternans
Main causes of acute pancreatitis
PANCREATITIS
hyperParathyroidism Alcohol Neoplasm Cholelithiasis Rx - NRTIs (didanosine, zalcitabine, stavudine), Ritonavir, Sulfanamides Ercp Abdominal surgery hyperTriglyceridemia Infection - mumps Trauma Idiopathic Scorpion sting - not in US
Presentation and Diagnostic testing for acute pancreatitis
Rapid onset of severe epigastric abd pain
- may radiate to back
- Worse with eating -> sitophobia
N/V
Intravascular depletion -> tachycardia, hypotension/shock, multi organ failure
Cullen/Grey turner sign
Dx:
Elevated lipase (and amylase) - not indicative of severity
Ranson critieria for severity/prognosis
Best radiology study: CT scan - enlarged, inflamed, may show pseudocyst
Abd XR: dilated loop of bowel near pancreas “sentinel loop”; elevation of diaphragm, pleural effusion
Ranson criteria
Severity of pancreatitis - one point for each
On admission: GA LAW Glucose >200 AST >250 LDH >350 Age >55 WBC > 16,000
During first 48 hours: CALvin and HOBBeS Serum calcium less than 8 Hematocrit decrease >10% paO2 less than 60 Base deficit >4 BUN increase >5 Sequestration of fluids >6L (bad sign)
0-2 points = 0-3% mortality
3-5 points = 11-15% mortality
6-11 points = >40% mortality
Management of acute pancreatitis
IVF NPO NG suction - ppx for N Correct electrolyte abnormalities Opioids for pain control - use meperidine (morphine can cause sphincter of Oddi spasms)
If not tolerating referring -> Nasojejunal feeding (won’t stimulate pancreas) or TPN
Cholecystectomy if caused by choledocholithiasis
Complications of pancreatitis
Respiratory failure Renal failure Shock Sepsis DIC Hemorrhage
Pancreatic necrosis, abscess, pseudocyst
Chronic pancreatitis
Most common cause of chronic pancreatitis
alcoholism
Symptoms suggestive of chronic pancreatitis
recurrent epigastric pain
N/V
Fat malabsorption/steatorrhea
Best lab test for diagnosing chronic pancreatitis
fecal elastase is low
XR/CT - calcifications, enlarged ducts
MRCP
Management of chronic pancreatitis
Stop etOH use Stop smoking Opioids for analgesia Pancreatic enzymes Vitamin supplements Small, low fat meals
Surgery to decompress dilated duct, resect part of pancreas
Complications of chronic pancreatitis
Pseudocysts - resolve on one, or drain if complications, pain or not resolving
Obstruction of bile ducts/duodenum
Malnutrition
glucose intolerance/DM
pancreatic cancer
Pancreatic pseudocyst vs true cyst
Pseudocyst: fluid contained by inflammatory tissue
Cyst - fluid contained by epithelial tissue
Complications of pancreatic pseudocyst
rupture abscess pseudo aneurysm - erosion into adjacent blood vessel with hemorrhage into pseudocyst -painful as it expands rapidly -dangerous
Test to distinguish pseudocyst from cystic pancreatic neoplasm
Aspirate fluid via CT guided percutaneous aspiration or endoscopic U/S needle aspiration
Pseudocyst fluid high in amylase
Systemic lupus erythematosis (SLE)
MC in women, AA
Onset black women 15-45, all others 40-60
Features: 4 out of 11 over time
- Malar rash
- Discoid rash
- Photosensitivity
- Painless oral ulcers
- Arthritis - inflammatory, non erosive, affects at least 2 joints
- Serositis - pericarditis, pleuritis, pleural effusion
- Renal disorders - glomerulonephritis, proteinuria, renal failure - cause of death
- Neurologic disorders - seizures, psychosis, peripheral neuropathy
- Hematologic disorders - hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia
- ANA high (1:160, 1:320)
- Immunologic disorder - anti-dsDNA, anti-Smith, antiphospholipid antibodies
Diagnostic testing:
ANA, anti-dsDNA, anti-Smith, antiphospholipid
Low C3 and C4
Anti-histone Ab - drug induced
Tx:
Avoid sun exposure
Hydroxychloroquine, NSAIDs, glucocorticoids
Complications:
- Hypercoagulability - lupus anticoagulant, anticardiolipin Ab, antiphospholipid Ab
- Immunocompromised
- CV disease
- Renal failure
Drugs associated with drug induced lupus
SHIPP
Sulfonamides Hydralazine Isoniazid Phenytoin Procainamide
Anti-histone Ab
Polymyalgia reumatica (PMR)
Strongly associated with Giant Cell Arteritis
MC: elderly women
Joint pain and stiffness in shoulders, neck, and/or hips
No muscular weakness
significantly elevated ESR and CRP
Anemia common
Negative serologic markers - ANA, RF
MRI or PET show synovial inflammation
Tx:
Low-dose glucocorticoids (15-20 mg/day) for 2-4 weeks, then gradual taper over 1-2 years
Polymyositis and dermatomyositis
Progressive, symmetric weakness of proximal limb muscles - hip flexors, shoulders, deltoids; trouble climbing stairs, raising hands over head
Minimal muscle soreness/tenderness
Skin manifestations in dermatomyositis:
- malar rash
- heliotrope rash on eyelids
- Gottron’s papules on knuckles, elbows, or knees
- Mechanic hands (hyperkeratosis and cracking of hands or feet)
- “Shawl sign” on shoulders
- “V sign” on anterior chest
Dx testing:
Elevated CK, ALT, AST, andaldolase
ANA frequently positive
ANTI-JO1 - antisynthetase Ab
EMG distinguishes muscle pathology from nerve pathology
MUSCLE BX - muscle fiber degeneration and inflammatory cells
Tx:
High dose glucocorticoids for 4-6 weeks, then gradual taper
Methotrexate or azathioprine - may reduce duration of glucocorticoid tx
Complication: risk of malignancy - breast, prostate, colon, lung
Fibromyalgia
Increased sensitivity to pain without specific cause
Risk: women 20-50
Assoc with inflammatory rheumatologist dz (RA, SLE), depression, IBS
Features:
Widespread muscle and joint swelling or inflammation
Multiple tender trigger points
Severe fatigue
Sleep disturbance
Depression or anxiety in at least 30% of patients
Cognitive disturbance - “fog”
Labs and XR normal
Tx: Non pharm: -Reassure -stretching exercises -sleep hygiene -Address psych issues - depression, anxiety, ptsd
Pharm: Acetaminophen and NSAIDS - avoid opiates Pregabalin SNRIs - fluoxetine, milnacipran, venlafaxine Sleep aids as needed
Systemic sclerosis (scleroderma)
Excess collagen deposition in skin and other tissues
Diffuse cutaneous systemic sclerosis
Limited cutaneous systemic sclerosis
Tx:
Supportive care - PPI, CCB, ACE-I
Tx severe skin sclerosis with methotrexate, mycophenolate, or cyclophosphamide
Diffuse cutaneous systemic sclerosis (dcSSc)
Widespread sclerosis involving skin and visceral organs
Progresses rapidly, early involvement of visceral organs
Skin may appear shiny and lack wrinkles - finger contractions and ulcerations
Assoc with anti-DNA topoisomerase 1 Ab - anti-Scl 70 and/or anti-RNA polymerase Ab
Limited cutaneous systemic sclerosis (lcSSc)
Skin involvement limited to hands +/- face and neck
Less visceral involvement; progresses less rapidly
CREST syndrome: Calcinosis cutis: calcifications in deep layers of the skin, often in fingers Raynaud phenomenon Esophageal dysmotility - LES sclerosis Sclerodactyly Telangiectasis - lips, hands, or face
Assoc with anti-centromere Ab
Sjogren syndrome
Exocrine glands
Clinical features:
Xerophthalmia - dryness, conjunctivitis, sensation of sand in eyes
Xerostomia - dysphagia, enlarged parotid glands, dental caries
Arthritis
Nasal dryness
Vaginal dryness
Dx:
Anti-SSA aka Anti-Ro Ab
Anti-SSB aka Anti-La Ab
Tx:
Dry eyes: artificial tears, cyclosporin eye drops
Dry mouth: muscarinic agonists - pilocarpine, cevimeline
Arthritis: hydroxychloroquine or methotrexate
Osteoarthritis aka DJD
Joint degeneration with erosion of articular cartilage
Risk: aging, obesity, joint injury
Features:
Noninflammatory arthritis of hips, knees, ankles, hands/feet, spine
Pain worse with use, better with rest
No systemic sxs
Assymmetric arthritis with boney enlargement of DIP joints (Heberden’s) and PIP (Bouchard’s)
Dx:
XR: osteophytes and joint space narrowing
ESR normal, no Ab
Tx: Prevent overuse, provide rest periods Wt loss Acetaminophen, NSAIDs, or celecoxib Glucocorticoid joint injections Hyaluronic acid joint injection Joint replacement for severe disease
Rheumatoid arthritis (RA)
Type III hypersensitivity reaction -> immune complexes deposited in tissues -> joint inflammation and pannus formation (synovial hypertrophy, granulation tissue on articular cartilage)
Risk: Women, HLA-DR4
Features:
Chronic inflammatory arthritis - hands, wrists, large joints
Morning stiffness
Pain and stiffness worse with rest, improves with use - gel phenomenon
Systemic sxs: subcutaneous nodules, pleuritis, pericardiits, scleritis
Swelling of MCPs and PIPs - Boutonniere and swan neck deformities
Ulnar deviation of fingers (away from thumb)
Dx:
elevated ESR and CRP
Positive RF - anti IgG Ab
Positive anti-citrullinated protein antibodies (ACPA)
Treatment of RA
DMARDs, with adjuncts of steroids or NSAIDs
Drugs in MSK treatment notecards
Psoriatic arthritis
Patterns of arthritis:
Assymetrical, inflammatory arthritis involving DIP joints
Symmetrical arthritis like RA
Severe, mutilating arthritis (arthritis mutilans)
Spondyloarthritis
Dactylitis - sausage fingers Anterior uveitis (inflammation of iris and ciliary bodies) or conjunctivitis
Dx:
HLA-B27
Seronegative (negative RF, ANA)
XR: fingers “pencil-in-cup” deformities
Tx:
NSAIDs or celecoxib
Methotrexate, leflunomide, or TNF alpha inhibitors
Ankylosing spondylitis
White Men 20-30s
LBP worse with inactivity, improves with exercise
Reduced spine mobility - abnormal Schober test
Possible hip and shoulder pain
Anterior uveitis - eye pain, blurred vision, photophobia
CV Dz - aortic regurg, conduction disturbances
Dx:
HLA-B27
Negative RF, ANA
XR pelvis - sacroilitis and SI joint fusion
XR L-spine - vertebral fusion “bamboo spine”
Tx:
PT and exercise
NSAIDs or celecoxib continuously
TNF alpha inhibitors
Paget disease of bone
Focal areas of excessive bone remodeling (overcast overactivity -> osteoblast overactivity)
-axial skeleton, long bones of legs
Presentation: asx or bone pain arthritis bone deformity - bowed tibias, kyphosis Increased risk of fx hearing loss increased skull circumference - hat doesn't fit
Dx:
Elevated alk phos - marker of osteoblast activity
XR: osteolytic lesions and hyper dense sclerotic lesions
Radionuclide bone scan: “hot spots”
Tx: bisphosphonates or calcitonin injections
Risk: osteosarcoma
Anterior shoulder dislocation
MC
Arm position: external rotation and slight abduction
Bankart lesion - Tears anterior labrum and capsule of shoulder
Axillary artery and nerve at risk
Classic scenario: Blow to abducted, externally rotated, extended arm - block a basketball shot
Physical exam: Prominent acromion (if thin pt), loss of shoulder roundness
Posterior shoulder dislocation
Arm position: internal rotation and adduction
Unable to externally rotate
XR: “light bulb” on AP view
Neurovascular compromise unusual
Classic scenario: blow to anterior shoulder, seizure, electrocution
Exam: posterior prominence and anterior shoulder is flat
Treatment of shoulder dislocation
Pain control:
glenoid cavity lidocaine injection
Narcotics
Conscious sedation
Reduce:
traction-counter traction
-Hippocratic, prone, scapular manipulation
Sling immobilization
Re xray
F/up with ortho - likely to dislocate again
Immune thrombocytopenia (ITP)
Caused by anti-platelet IgG Ab
Could be primary ITP, Or secondary (HIV, hepatitis C, lupus, CLL)
Platelet count often below 50,000
Treatment -
Children: not necessary
Adults: glucocorticoids or IVIG; platelet transfusion for significant bleeding
Drugs known to cause thrombocytopenia
Heparin Abciximab (GP IIb/IIIa inhibitor) Carbamazepine, Phenytoin, valproate Cimetidine Acyclovir Rifampin Sulfonamides (sulfasalazine, TMP-SMX) Procainamide, quinidine Quinine
Heparin-induced thrombocytopenia (HIT)
Thrombosis plus thrombocytopenia - sudden decrease in platelet count by at least 50%
Heparin forms complexes with platelet factor 4
Antibodies against the complex cause platelet activation and aggregation -> risk thrombosis
Platelets are removed from circulation
Diagnostic testing:
ELISA detects platelets
Serotonin release assay- Gold standard but expensive
Heparin-induced platelet aggregation assay - specific not sensitive
Treatment:
Stop heparin
Anticoagulate with direct thrombin inhibitor, (argatroban) warfarin x3 mo
Lifelong avoidance of heparin and LMWHs
Thrombotic thrombocytopenia purpura - hemolytic uremic syndrome (TTP-HUS)
Enzyme deficiency -> unregulated platelet aggregation -> thrombosis
Consumption of platelets -> thrombocytopenia
Thrombosis-> Microangiopathic hemolysis
E coli O157:H7 - kids
HUS:
Hemolysis
Uremia (renal failure)
Thrombocytopenia
TTP: Hemolysis Uremia (Renal failure) Thrombocytopenia Neurological sequelae - AMS, seizures, coma Fever - high
Treatment:
Plasma exchange plus glucocorticoids
HELLP syndrome
Sequelae of preeclampsia
Presentation: Hemolysis Elevated liver enzymes low platelets Hypertension
Treatment
Induce labor and deliver
Thrombocytopenia caused by impaired platelet production - causes
Infections: parvovirus b19, other viruses
Megaloblastic anemia - folate/b12 deficiency
Alcohol abuse - directly toxic to bone marrow
Thrombocytopenia caused by splenic sequestration of platelets - findings
Splenomegaly
Bone marrow biopsy is normal
Splenectomy curative
Multiple myeloma
Malignant monoclonal perforation plasma cells
Clinical features:
Normocytic anemia
Bone pain, back pain, pathological fractures
Hypercalcemia -> constipation, abdominal pain, encephalopathy, polyuria, dehydration
Kidney disease (light chain cast nephropathy “myeloma kidney”)
Fatigue
Weight loss
Recurrent infections
Vertebral compression fractures -> radiculopathy or cord compression
Dx:
Serum protein electrophoresis (SPEP) - M spike (gamma) - usually IgG may be IgA
UPEP - Bence Jones proteins
Skeletal survey shows lytic lesions due to local osteolytic factors - punched out
Bone marrow biopsy shows increase plasma cells
Tx:
Cytogenetic testing -> prognosis, timing of tx
Chemo (lenalidomide) + bone marrow transplant (if aggressive)
Hodgkin’s lymphoma
B cell lymphoma - Reed-Sternberg cell - large binucleated cells with prominent nucleoli and clearing around cell
-background of reactive lymphocytes and granulocytes
Bimodal age: 20 and 65
Clinical features:
Painless cervical lymphadenopathy - firm, rubbery
B symptoms: low-grade fever, night sweats, weight loss
Pruritus
Dx:
CXR or CT - mediastinal lymphadenopathy
4 subtypes: Nodular sclerosis (MC), Lymphocyte-rich, lymphocyte-depleted, mixed cellularity
Tx:
Chemo+rad
Hematopoetic cell transplants for relapse or progression despite chemo/rad
Nodular sclerosis subtype of Hodgkin’s lymphoma
Most common subtype
Nodules of lymphocytes separated by sclerotic bands a collagen
Relatively few R-S cells
Good prognosis
Lymphocyte rich subtype of Hodgkin’s lymphoma
Please common subtype
Few R-S cells
Best prognosis
Lymphocyte depleted subtype of Hodgkin’s lymphoma
Abundant R-S cells
Poor prognosis
Mixed cellularity subtype of Hodgkin’s lymphoma
Second most common subtype
Mix of lymphocytes and R-S cells without nodules or sclerotic bands
Non-Hodgkin’s lymphoma
lack Reed-Sternberg cells
Presentation:
Pain is generalized lymphadenopathy
Constitutional “B” symptoms - fever, night sweats, weight loss
Diffuse large B cell lymphoma
Most common non-Hodgkin’s lymphoma
More common in elderly men
lymphoblastic lymphoma
Most common non-Hodgkin’s lymphoma in children
Follicular lymphoma
Second most common non-Hodgkin’s lymphoma overall
90% have t(14;18)
“Cleaved cells” - lymphocyte looks like a heart
Burkitt lymphoma
Associated with t(8;14)
Three forms: sporadic, endemic (EBV in Africa - mandible), immunodeficiency associated (HIV)
“starry sky” appearance on bx
Small lymphocytic lymphoma
Malignant cells are identical to chronic lymphocytic leukemia
Harry cell leukemia
Classified as a lymphoma
Malignant cells have “Harry” cytoplasmic projections
Causes of polycythemia
Hypoxemia
- COPD
- Live at altitude
Inappropriate elevated epo (tumors)
- Pheo
- RCC
- HCC
- Hemangioblastoma
Classic presentation of polycythemia vera
Hyper viscosity causing vascular sludging
Visual disturbances: blurred vision, amaurosis fugax, scintillating scotoma, ophthalmic migraine
Thrombosis: stroke, MI or angina, DVT or PE, Budd-Chiari syndrome, superficial thrombophlebitis
Erythromelalgia - Burning pain in the hands and feet with erythema, pallor or cyanosis
Pruritis - especially after a warm bath
Facial plethora - reddening of the face
Hepatosplenomegaly
Elevated H&H and RBC mass, leukocytosis (40%), thrombocytosis (60%)
Treatment of polycythemia vera
Phlebotomy to keep hematocrit below 45% males, 42% females
->desirable iron deficiency anemia - do not supplement iron!
Add hydroxyurea if at high risk for thrombosis (over age 70, and prior thrombosis, platelets >1,500,000, or CV risk factors)
Aspirin every day to help prevent thrombosis (MI, CVA, PE, DVT)
Anterior cerebral artery (ACA) - region supplied, results of stroke
Medial cortex - frontal and parietal lobes
Motor/sensory defects of lower extremity and trunk
Middle cerebral artery (MCA) - region supplied, results of stroke
Lateral cortex - parietal and temporal lobes
Motor/sensory deficits of face and upper extremity, Aphasia
Posterior cerebellar artery(PCA) - region supplied, results of stroke
Occipital lobe
Impaired vision
Parkinson disease
Degeneration of dopaminergic neurons in the substantia nigra
- decreased dopamine + relative increase in ACh
- Lewy bodies: eosinophilic conclusions of alpha-synuclein and ubiquitin (halo around)
Risk factors: Family history Advancing age Head trauma MPTP (methyl-phenyl-tetra-hydropuridine) - byproduct of meperidine synthesis -> metabolized to MPP (methyl-phenyl-perideium) -> damage to substantia nigra
Features:
Decreased movement (bradykinesia, hypokinesia, akinesia)
Postural instability
Fenestrated gait
Resting tremor (pill rolling)
cogwheel rigidity
Mask like facies (hypokinesia of facial muscles)
Autonomic dysfunction, orthostatic hypotension
Cognitive dysfunction, dementia, depression, apathy
Clinical diagnosis
Amyotrophic lateral sclerosis (ALS)
Features:
Weakness with normal sensation
Initial presenting symptoms:
-asymmetrical in weakness - hands, fingers, shoulder girdle, lower extremity (foot drop), or pelvic girdle
-Bulbar dysfunction (dysarthria or dysphasia) - medulla involvement
UMN S/S:
movement stiffness, slowness and incoordination
Spasticity and hyperreflexia (spastic paralysis)
Slow rapid alternating movements - dysdiadochokinesia
Gait disorder
Bulbar UMN S/S:
Dysarthria, dysphasia
pseudobulbar affect - inappropriate laughing, crying, or yawning
LMN S/S: Weakness, gait disorder Reduced reflexes (flaccid paralysis) Muscle atrophy Fasciculations
Cognitive deficiets: frontotemporal executive dysfunction
Neuromuscular respiratory failure months to years after dz
avg survival - 3-5 yrs
Dx:
EMG: widespread acute and chronic muscular denervation and reinnervation
Tx:
Riluzole - slows progression of ALS and prolonged survival by decreasing glutamate-induced excitotoxicity
Normal pressure hydrocephalus (NPH)
Inflammation and fibrosis of the arachnoid granulations -> and impaired reabsorption of CSF -> excess CSF builds up in the ventricles
Presentation: (3 W’s)
Wacky - cognitive impairment
Wet - urinary incontinence
Wobby - gait disturbance - magnetic, early sign
Dx:
MRI: dilation of the cerebral ventricles and enlargement
CSF pressure not elevated
Tx: ventricular shunting
Delirum - Daily course: Onset: Memory: Level of consiousness: Visual hallucinations: Prognosis:
Daily course: waxes and wanes in a day Onset: acute - hours to days Memory: impaired Level of consiousness: decreased Visual hallucinations: common Prognosis: reversible
Dementia - Daily course: Onset: Memory: Level of consiousness: Visual hallucinations: Prognosis:
Daily course: consistent, Sundowning (more confused in evening) Onset: gradual Memory: impaired Level of consiousness: normal Visual hallucinations: uncommon Prognosis: generally irreversible
Diabetes insipidus
Disorder of ADH directed water reabsorption -> dehydration and hypernatremia
Central vs nephrogenic vs lithium induced
Presentation: polyuria, polydipsia
Labs: High serum sodium High serum osmolality Variable urine sodium - usually low low urine osmolality Water deprivation test - urine osmolality stays low despite water restriction
Tx:
treat underlying condition
Lithium induced - HCTZ + amiloride
Central diabetes insipidus
Posterior pituitary stops producing ADH
Causes: Brain trauma, destructive pituitary tumors, hypoxic encephalopathy, anorexia nervosa, idiopathic
Supplement ADH (desmopressin) -> increased urine osmolality
Tx: desmopressin
Nephrogenic diabetes insipidus
Kidneys are unresponsive to ADH
Causes: hereditary renal disease, lithium toxicity, hypercalcemia, hypokalemia
supplement desmopressin - urine osmolality stays low
Tx:
Restrict dietary salt
HCTZ
indomethacin
Lithium - HCTZ + amiloride
Hyperkalemia
Causes: Metabolic acidosis adrenal insufficiency aldosterone deficiency Tissue breakdown Insulin deficiency Renal failure Potassium sparing diuretics
ECG:
Tall peaked T waves
Can predispose to ventricular tachycardia and asystole
Condition shifting potassium out of cells
leads to hyperkalemia
Low insulin Beta blockers Acidosis digoxin cell lysis
Condition shifting potassium into cells
Leads to hypokalemia
Insulin
Beta agonists - albuterol
Alkalosis - sodium bicarb
Cell creation/proliferation
Emergency treatment for hyperkalemia
Stabilize cardiac membranes - IV calcium gluconate or IV calcium chloride
Drive potassium into cells
- insulin + D50
- beta agonist - albuterol, nebulized
- sodium bicarb
Remove potassium from the body
Hemodialysis
Sodium polystyrene sulfonate (Kayexalate)
Loop diuretics - chronic
Hypokalemia
Causes: Poor dietary intake Alkalosis Hypothermia Vomiting Diarrhea Hyperaldosteronism Insulin access Diuretics RTA 1 or II (renal tubular acidosis)
Presentation: Fatigue and weakness Hyporeflexia Possible paralysis or parathesias if severe Arrhythmias
ECG:
T wave flattening
ST depression
U waves
Tx:
Treat underlying disorder
Give oral or IV potassium - need central line to avoid sclerosing of veins
Avoid overly rapid replacement
Hypercalcemia
Corrected serum calcium or get ionized:
total serum calcium + (0.8 x (4-albumin))
Causes:
Hyperparathyroidism
Neoplasms - PTHrP (squamous cell lung ca), lytic bone dz
Thiazide diuretics
Milk-alkali syndrome - Ca carbonate antacids + mlik, Ca supplements
Sarcoidosis - macrophages generate vitamin D
Vitamin a toxicity
Presentation: Bone pain Fractures Nephrolithiasis Nausea/vomiting PUD Constipation Weakness Mental status changes Polyuria can cause acute pancreatitis
Labs: +/- increased PTH
ECG: shortened QT interval
Tx:
Hydration!!!
Calcitonin, bisphosphonates, Glucocorticoids
Surgery - hyperparathyroidism, resect neoplasms
Hypocalcemia
Causes: Hypoparathyroidism Hyperphosphatemia Chronic renal failure Vitamin D deficiency Loop diuretics Pancreatitis Alcoholism
Presentation: Tingling of the lips and fingers paresthesias Carpal and pedal spasms "cramping" Tetany Laryngeal spasm with difficulty breathing Seizures Chvostek's sign - cheek Trousseau's sign
ECG: QT prolongation
Tx:
Treat underlying disorder
PO or IV calcium
Vit D supplements
Winters formula
pCO2 = 1.5 (HCO3) + 8 +/-2
predict pCO2 in metabolic acidosis with respiratory compensation
If measured pCO2 differs from predicted, indicates mix disorder rather than simple respiratory compensation
Causes of metabolic alkalosis
Vomiting - lose H+ Diuretics - contraction alkalosis (lose water relative to bicarb) Cushing syndrome Hyperaldosteronism Adrenal hyperplasia Volume contraction
Causes of respiratory alkalosis
Hyperventilation Asthma Pulmonary embolism High-altitude Aspirin toxicity - directly stimulates respiratory center in brain, early
Causes of metabolic acidosis - high anion gap
Methanol Uremia DKA Propylene glycol Isoniazid/iron Lactic acidosis Ethylene glycol Salicylates - late aspirin toxicity finding
Cause of metabolic acidosis normal anion gap
Diarrhea - MC Renal tubular acidosis TPN Hyperaldosteronism - type 4 RTA Addison disease
Causes of respiratory acidosis
COPD - retain CO2
Respiratory depression - Brain injury
Neuromuscular diseases
Opioid overdose
Differential diagnosis of normal anion gap metabolic acidosis with hypokalemia
Renal tubular acidosis types I and II Diarrhea Fanconi syndrome (type II RTA)
Differential diagnosis of normal anion gap metabolic acidosis with hyperkalemia
Addison disease
Renal tubular acidosis type IV
Hyperalimentation (TPN)
Renal tubular acidosis (RTA) type 1
Distal
Impaired H+ secretion in collecting tubules (intercalated cells)
Causes: autoimmune diseases Drugs Infection Cirrhosis SLE obstructive nephropathy
Urine pH - high - over 5.3
Labs: low K
Calcium kidney stones
Tx:
Oral HCO3
K supplements
Thiazide diuretics
Renal tubular acidosis (RTA) type 2
Proximal
Impaired bicarb reabsorption in the PCT
Causes: Multiple myeloma, amyloidosis - excess proteins and urine Fanconi syndrome Wilson disease Vitamin D deficiency Autoimmune diseases
Urine pH normal, below 5.3
Labs: low K, low HCO3
Tx:
Oral HCO3
K supplements
Thiazide diuretics
Renal tubular acidosis (RTA) type 4
hypoaldosteronism -> impaired potassium secretion
Principle cells of collecting tubules
Causes: Addison disease
Urine pH - less than 5.3 (normal)
Labs: hyperkalemia, normal HCO3
Tx: fludrocortisone, K restriction
Febrile seizures
6 mo - 6 y
Absence of CNS infection/lesion
Presentation:
tonic-clonic seizure less than 15 minutes, first day of illness
Postictal state less than 5-10 min
Tx- lower temp, reassure, no antiepiletics
-if seizure witnessed and lasting >5 min - IV diazepam or lorazepam, or buccal midazolam if no IV access
Testing not needed - LP if meningitis suspected
1-2% develop epilepsy, 40% will have another within 2 years
