Final Exam Review Flashcards
1
Q
Causes anion gap metabolic acidosis
A
MUDPILES CAT
* methanol
* uremia
* DKA
* propylene glycol
* Iron, Isoniazid
* Lactic Acidosis
* Ethanol
* Salicylates (ASA)
* Carbon Monoxide
* Aminoglycosides
* Theophylline
no change in chloride
2
Q
causes of non-anion gap metabolic acidosis
A
- hyperalimentation
- Addison’s
- Renal tubular acidosis
- diarrhea
- acetazolamide
- spironolactone
- saline infusions
compensatory increase in Cl-
3
Q
causes of chloride responsive metabolic alkalosis
A
- vomiting
- NG suctioning
- diuretics
- volume depletion
- laxative abuse
4
Q
causes of chloride unresponsive metabolic alkalosis
A
- Aldosteronism (Conn Syndrome)
- Bartter’s syndrome
- Cushing’s syndrome
- depleted Mg
5
Q
Pneumonia (everything)
A
- Patho: pneumonia acquired in the community or w/in 48 hrs of hospitalization, can be bacterial (s. pneumoniae, MRSA, or atypical), viral (rhinovirus, coronavirus, RSV), fungal (histoplasmosis, coccidiomycosis, or PJP); the cough can be productive (most), dry (atypical bacteria), or blood tinged (MRSA).
- sx: dyspnea, pleuritic CP, HA, fever, malaise, myalgia, arthralgia; PE findings include increased RR, signs of resp distress (accessory muscle use), increased fremitus, dullness to percussion, and crackles/bronchial sounds
- dx: is via CXR which shows multilobar infiltrates (s. pneumoniae, legionella), interstitial infiltrates (viral, mycoplasmas), or cavitation (mycoplasmas, s. aureus, fungals) if CXR is negative you can do CT if you still have high clinical suspicion
- tx: for outpatient is amoxicillin unless comorbidities then Augmentin + macrolide, inpatient is beta lactam + macrolide/fluoroquinolone, ICU pts should get inpt tx or macrolide + fluoroquinolone; if worried about MRSA give vancomycin or linezolid; if worried about p. aeruginosa give piperacillin-tazobactam.
6
Q
Sickle Cell
everything
A
- patho: autosomal recessive inherited disorder characterized by hemoglobin S which causes RBCs to be sickle shaped and elongated; trait = heterozygous, can be asx and disease = homozygous and severe disease;
- sx: include classic sx of anemia, delayed growth/puberty, short stature, frequent infections, and pain (dactylitis= pain in feet/hands) ; PE findings include organomegaly (jaundice), cardiomegaly (hyperdynamic precordium, systolic murmur), retinopathy, and slow healing LE ulcers
- dx: is via neonatal testing, CBC (low hgb, low hct, increased platelets, WBCs), smear (sickle RBCs, NRBCs, Howell-Jolly bodies), sickle solubility test (turbid blood), hgb electrophoresis (which shows increased Hgb S)
- tx; is lifelong transfusions w/ iron chelation to prevent iron overload, omega-3 fatty acid and folate supplementation, hydroxyurea, and crizanlizumab; bone marrow transplant is curative.
7
Q
emphysema phenotype
A
- patho: alveolar damage leading to neutrophil response leading to proteases leading to anti-protease activity results in alveolar destruction, reduced elasticity, air trapping in alveoli
- sx: include “pink puffer” (7 things) sx of barrel chestedness, infrequent cough, hyperresonance, wt loss, pursed lip breathing, intercostal muscle use, and tripod positioning.
8
Q
chronic bronchitis phenotype
A
- pathophys involves decreased effectiveness of mucociliary movement due to inflammation leading to hypersecretion of mucus which plugs the bronchi ultimately leading to scarring and fibrosis
- sx include “blue bloater” sx of cyanosis, edema, wt gain, wheezing/rhonchi, and chronic productive cough.
9
Q
COPD overview + Management
A
- obstructive lung disease;
- heterogenous;
- general sx include chest tightness, dyspnea, and morning HAs; PE findings include hyperresonance, cyanosis, nail clubbing, barrel chest, wheezing, prolonged expiration, cor pulmonale (eventually), and signs of resp distress;
- dx is via PFTs (increased TLC, FEV1:FEVC < 0.7, obstructive pattern), CXR (hyperinflated, black, reduced pulm vasculature, flattened diaphragm, wide ribs), and other misc tests (AAT, ABG);
- pts are classified based on GOLD standards into group A (mild sx, low risk of exacerbation), group B (mod/high sx, mod risk of exacerbation), and group E (mod sx, highest risk of exacerbation)
- tx varies by group A (SABA + SAMA), group B (SABA rescue + LAMA + LABA), and group E (SABA rescue + LAMA + LABA + ICS).
10
Q
eosinophilic esophagitis
A
- irritation of entire esophagus due to T2 helper T-cell mediated cytokine (IL-5, IL-13, exotoxin) release
- sx are similar to GERD but are unresponsive to PPIs and antacids
- dx is after failing 8wk trial of PPIs and involves endoscopy biopsy (>15 eosinophils per HPF with eosinophil predominant inflammation throughout entire esophagus) and imaging (trachealization, white papules indicative of micro abscesses, mucosal fragility, strictures, and linear burrows), pts will also have elevated IgE
- tx includes trialing food elimination diets (seafood, cereals, nuts, eggs, dairy), PO or inhaled corticosteroids (8wks), duplimab (gold standard in >1 yr), and surgical option is balloon dilation.
11
Q
Hemophilia A
A
- caused by deficiency of Factor VIII; X-linked recessive disorder so primarily affects men and women are carriers
- sx include spontaneous bleeds, muscle/GI bleeds, and hemarthroses
- dx is via aPTT which is prolonged and decreased Factor VIII levels
- tx is desmopressin and Factor VIII replacement.
B is factor 9; C is factor 11
12
Q
Autoimmune Hemolytic Anemia
A
- extravascular hemolytic anemia; occurs due to autoimmune antibodies against RBCs OR autoimmune antibodies against another structure which leads to the destruction or damage of RBCs
- warm disease meaning RBC destruction occurs at body temp, IgG mediated disorder
- sx include a rapidly progressing anemia, splenomegaly, jaundice; may be secondary to beginning a new medication or infection
- dx is a positive direct Coomb’s test, smear shows spherocytes, reticulocytes are increased, LDH is increased, haptoglobin is decreased
- acute tx is steroids (prednisone PO) and plasmapheresis
- alternative tx includes rituximab, IVIG, or splenectomy.
13
Q
Cold Agglutinin Disease
A
- characterized by cold associated complement mediated RBC destruction; IgM mediated
- sx include low back pain, hematuria after cold exposure, acrocyanosis (blue hands/feet), and numb/mottled hands/feet
- dx involves serum cold agglutinin titers (positive), CBC (increased LDH, decreased haptoglobin, increased reticulocytes, mild anemia), smear (agglutinated RBCs)
- tx is avoidance of the cold, rituximab, and PRN RBC transfusions (must be warmed).
14
Q
Compartment Syndrome
A
- increased pressure within the fascial compartment of a muscle; risk factors include major surgeries, fractures, crush injuries, and tight casts/dressings
- sx in adults include the 6 P’s (pain [worse w/ stretching of muscle], pallor, paresthesia [loss of sensory function first then motor], paralysis, pokilothermia [variable core body temp], and pulselessness
- in peds the sx include the 3 A’s (agitation, analgesia, and anxiety)
- dx is via intra-compartmental pressure monitoring (if >30mmHg single compartment read or if DBP-compartment pressure < 30mmHg)
- tx is emergent fasciotomy w/in 1 hr of dx to alleviate pressure in the compartment.
15
Q
Multiple Myeloma
A
- malignancy of hematopoietic stem cells (plasma cells); causes increase IgG or IgA production within the marrow
- sx include lytic lesions on bones (leading to bone pain/osteoarthritis), AKI (weakness, peripheral edema, SOB), hypercalcemia (stones, thirst, urination, constipation, confusion), hyper-viscosity, CNS sx (numbness, weakness, back pain), and increased rate of infections (s. pneu or h. flu)
- dx involves serum protein electrophoresis (SPEP), Bence-Jones Protein in urine, and a skeletal Xray to look for lytic lesions
- tx is dexamethasone, immunomodulators, and proteosome inhibitors; can give bisphosphonates to improve bone strength.
