Adam Shared "To Do" - 73 Picmonics

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To Do

Pyruvate dehydrogenase complex
Mitochondrial enzyme complex linking glycolysis and TCA cycle
Differentially regulated in fed/fasting states (active in fed state)
Reaction: pyruvate + NAD + CoA toŽ acetylCoA + CO2 + NADH
Complex is similar to the α-ketoglutarate dehydrogenase complex (same cofactors, similar substrate and action), which converts α-ketoglutarate toŽ succinyl-CoA (TCA cycle)
Arsenic inhibits lipoic acid. Findings: vomiting, rice-water stools, garlic breath
Cofactors
Thiamine pyrophosphate (B1 )
Lipoic acid
Lipoamide carries acyl groups
CoA (B5, pantothenic acid)
FAD (B2, riboflavin)
NAD (B3, niacin)
Activated By
High NAD+/NADH ratio, ADP, Ca2+
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Urea Cycle
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Lenticulostriate Artery (Turned to Lacunar stroke I believe, double check)
Affecred areas: Striatum, internal capsule
Contralateral paralysis and/or sensory loss—face and body. Absence of cortical signs (eg, neglect, aphasia, visual field loss).
Common location of lacunar infarcts, 2° to unmanaged hypertension and diabetes
Hypertension causes lipohyalinosis (hyaline deposition in arteries followed by foamy macrophages)
Microarethomas (atherosclerotic accumulation of foamy macrophages)
Both lipohyalinosis and microarethomas causes infarction leading to fluid filled cavities
May affect the subthalamic nucleus and cause hemibalism
If internal capsule involved --> pure motor stroke
If thalamus involved --> pure sensory stroke
Acute hemorrhage appears hyperdense on noncontrast head CT scan
Can cause Dysarthria-clumsy hand
Can affect the corona radiata, Pons, basal ganglia
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Herniation Syndromes
Cingulate (subfalcine) herniation under falx cerebri
Can compress anterior cerebral artery
Downward transtentorial (central) herniation
Caudal displacement of brain stem causesŽ rupture of paramedian basilar artery branches casuingŽ Duret hemorrhages; Usually fatal
Hemorrhages occur in the pons and midbrain
Uncal herniation
Uncus = medial temporal lobe. Compresses ipsilateral CN III (blown pupil, “down-andout” gaze), ipsilateral PCA (contralateral homonymous hemianopia with macular sparing)
Ipsilateral hemiparesis (due to contralateral corticospinal tract damage)
Contralateral crus cerebri at the Kernohan notch (ipsilateral paresis; a “false localization sign"
Displacement of the temporal lobe uncus under the tentorium cerebeli
Change In LOC (Altered Mental Status)
Cerebellar tonsillar herniation into the foramen magnum
Coma and death result when these herniations compress the brain stem
Cardiopulmonary arrest
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Psychiatric Treatments
Specific phobia - systematic desensitization
Postpartum depression - CBT and SSRIs are first line
Adjustment disorder - CBT, SSRIs
Postpartum psychosis - hospitalization and initiation of atypical antipsychotic; if insufficient, ECT may be used
U: antidepressants and mood stabilizer; don't leave alone with baby!
Panic disorder - CBT, SSRIs, and venlafaxine are first line. Benzodiazepines occasionally used in acute setting
#1 treatment is an SSRI (better than CBT but combination is best)
Social anxiety disorder - CBT, SSRIs, venlafaxine. For only occasional anxiety-inducing situations, benzodiazepine or β-blocker
Agoraphobia - CBT, SSRIs, MAO inhibitors
Generalized anxiety disorder - CBT, SSRIs, SNRIs are first line. Buspirone, TCAs, benzodiazepines are second line
Starting doses should be low to minimize initial activating side effects (for SSRI/SNRI)
#1 treatment is CBT (better than SSRIs but combo is best)
Obsessive-compulsive disorder - CBT, SSRIs, and clomipramine are first line
#1 treatment is CBT (better than SSRIs but combo is best)
Body dysmorphic disorder and acute stress disorder - CBT, SSRI
Post-traumatic stress disorder - CBT (trauma focused), SSRIs, and venlafaxine are first line; prazosin for PTSD nightmares
Edit PTSD
Bipolar disorder - Lithium, valproic acid, atypical antipsychotics
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Aliskiren
Direct renin inhibitor
Blocks conversion of angiotensinogen to angiotensin I
Indication
Hypertension
Side effects
Hyperkalemia
Decreased GFR
Hypotension
Relatively contraindicated in patients already taking ACE inhibitors or ARBs
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Hydronephrosis
Distention/dilation of renal pelvis and calyces (Pictured)
Usually caused by urinary tract obstruction (eg, renal stones, BPH, cervical cancer, injury to ureter ie surgery for histerectomy)
U. Ureter damage during pelvic surgery
Other causes include retroperitoneal fibrosis, vesicoureteral reflux
Dilation occurs proximal to site of pathology
Serum creatinine becomes elevated only if obstruction is bilateral or if patient has only one kidney
Leads to compression and possible pressure atrophy of renal cortex and medulla
Associated with increasted EPO, horseshoe kidney,
In neonate the ureteropelvic junction is a site of narrowing/kinking of the ureter that can cause hydronephrosis
Presents with palpable abdominal mass which is due to an enlarged kidney
S haematobium
U. Can lead to hypertension and sepsis; symptoms: pain, lower extremity edema, palpable kidneys or bladder
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Squamous Cell Carcinoma of the Bladder and Adenocarcinoma
Squamous Cell Carcinoma
Chronic irritation of urinary bladder causesŽ squamous metaplasia leading toŽ dysplasia and squamous cell carcinoma
Risk factors include Schistosoma haematobium infection (Middle East), chronic cystitis (older women), smoking, chronic nephrolithiasis
Presents with painless hematuria
Adenocarcinoma
Malignant gland proliferation usually within the bladder
Can arise from urachal remnant (at the dome of the bladder), cystitis glandularis or exstrophy of the bladder
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Urinary Tract Infection (Acute Bacterial Cystitis)
Inflammation of urinary bladder
Presents as suprapubic pain/pressure, dysuria, urinary frequency, urgency. Systemic signs (eg, high fever, chills) are usually absent
Risk factors include female gender (short urethra), sexual intercourse (“honeymoon cystitis”), indwelling catheter, diabetes mellitus, impaired bladder emptying
Benign prostatic hyperplasia
E coli (most common)
Staphylococcus saprophyticus—seen in sexually active young women (E coli is still more common in this group), second most common
Klebsiella (third most common)
Proteus mirabilis (urine has ammonia scent)
Enterococcus faecalis
Pseudomonas
Citrobacter (gram negative rod, slow lactose fermenter)
Lab findings: ⊕ leukocyte esterase. ⊕ nitrites (indicate gram ⊝ organisms, especially E coli). Sterile pyuria and ⊝ urine cultures suggest urethritis by Neisseria gonorrhoeae or Chlamydia trachomatis
Gonorrhea and chlamydia can present with urethritis
Urinalysis - cloudy urine with > 10 WBCs/High power field (HPF) alt naming pyuria of urine
Culture - Greater than 100,000 colony forming units (gold standard)
Leukocyte esterase = significant pyuria, nitrites = presence of Enterobacteriaceae (converts urinary nitrates to nitrites)
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Acute Pyelonephritis
Neutrophils infiltrate renal interstitium (Pictured, A)
Affects cortex with relative sparing of glomeruli/vessels
Presents with fevers, flank pain, nausea/vomiting, chills
Causes include ascending UTI (E coli is most common), vesicoureteral reflux, hematogenous spread to kidney
Other risk factors include indwelling urinary catheter, urinary tract obstruction, diabetes mellitus, pregnancy
Kidney stones
BPH (Benign Prostatic Hyperplasia)
Enterococcus faecalis and Klebsiella
Presents with WBCs in urine +/− WBC casts (WBCs precipitate with Tamm-Horsfall protein); leukocytosis
CT would show striated parenchymal enhancement (Pictured, B)
Complications include chronic pyelonephritis, renal papillary necrosis, perinephric abscess, urosepsis
Treatment: antibiotics
S haematobium
Dysuria, frequency, urgency, bacturia, costovertebral tenderness
Can be sterile pyuria in the case of Chlamydia or ureaplasma
Perinephric fat stranding
Most common pathogen is Escherichia coli (80%), but Proteus mirabilis , Klebsiella pneumoniae , and Staphylococcus saprophyticus as well
Urine culture is required for definitive identification
Complicated pyelonephritis
Progression to renal corticomedullary abscess , perinephric abscess , emphysematous pyelonephr itis, or papillary necrosis
Patients can develop sepsis with multiorgan failure, shock ,and renal failure
Risk factors: diabetes, kidney stones, immunosuppression, or other anatomic abnormalities of the urinary tract
These patients usually require imaging to evaluate for these complications, urological evaluat ion, and prompt therapy (medical/surgical)
Imaging is typically reserved for patients with persistent clinical symptoms despite 48-72 hours of therapy
History of nephrolithias is, or unusual urinary findings (eg, gross hematuria, suspicion for urinary obstruction).
Emphysematious (gas producing) pyelonephritis is much more common in diabetics and can be slow onset or abrupt (same symptoms as pyelo +/- abd pain)
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Chronic Pyelonephritis
The result of recurrent episodes of acute pyelonephritis
Typically requires predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones, BPH or cervical carcinoma
Coarse, asymmetric corticomedullary scarring, blunted calyces
Tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney) (Pictured)
Vesicoureteral reflux causes upper and lower pole scarring
Waxy casts may be seen in urine (Only according to Pathoma, not even google)
Interstitial fibrosis and atrophy of the tubules
U. has the appearance of dilated calyces
Xanthogranulomatous pyelonephritis
Rare
Characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages
Grossly orange nodules that can mimic tumor nodules
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Renal Osteodystrophy
Hypocalcemia, hyperphosphatemia, and failure of vitamin D hydroxylation associated with chronic renal disease
2° hyperparathyroidism
Hyperphosphatemia independently decreases serum Ca2+ by causing tissue calcifications
Decreased 1,25-(OH)2 D3 causing decreased intestinal Ca2+ absorption
1-alpha hydroxylation usually occurs in the proximal convoluted tubule
Causes subperiosteal thinning of bones
Can cause osteopenia, osteomalacia or undergo a similar process to primary hyperparathyroidism (osteitis fibrosa cystica)
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Acute Kidney Injury (Acute Renal Failure)
Acute kidney injury is defined as an abrupt decline in renal function as measured by increased creatinine and BUN; oliguria is common
Prerenal azotemia
Decreased RBF (eg, hypotension or HF) Ždecreases GFR
Na+/H2O and BUN retained by kidney in an attempt to conserve volume
Increased BUN/creatinine ratio (BUN is reabsorbed, creatinine is not) and decreased FENa
Intrinsic renal failure
Acute tubular necrosis or ischemia/toxin cause; less common acute glomerulonephritis (eg, RPGN, HUS) or acute interstitial nephritis
In ATN, patchy necrosis Žcausing debris obstructing tubule and fluid backflow across necrotic tubule Ždecreasing GFR
Urine has epithelial/brown granular casts
BUN reabsorption is impaired Ždecreasing BUN/creatinine ratio
Aminoglycosides, lead, myoglobinuria (muscle crush injury), ethylene glycol (oxalate crystals in urine), radiocontrast dye, urate (tumor lysis syndrome)
Hyperkalemia and metabolic acidosis
Persistent oliguria for 2-3 weeks due to tubular cells being stable cells that take time to reenter the cell cycle
Postrenal azotemia
Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies)
Develops only with bilateral obstruction
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Consequences of Renal Failure
Inability to make urine and excrete nitrogenous wastes
Can be caused by acute renal failure or chronic (eg, hypertension, diabetes mellitus, congenital anomalies, glomerular disease)
Treatment: Dialysis (can cause shrunken cystic kidneys with increased renal cell carcinoma risk)
MAD HUNGER
Metabolic Acidosis
Dyslipidemia (especially increased triglycerides)
Hyperkalemia
Uremia - clinical syndrome marked by increase in BUN
Nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction
Increased bleeding time (urea impairs aggregation), normal platelet count, PT and PTT
Urea crystals deposited in skin
Na+/H2O retention (HF, pulmonary edema, hypertension)
Growth retardation and developmental delay
Erythropoietin failure (anemia) which is usually produced by renal peritubular interstitial cells
Renal osteodystrophy (due to secondary hyperparathyroidism), osteomalacia, osteoporsis, bone pain, fractures
Can cause osteitis fibrosa cystica from secondary hyperparathyroidism
Hypocalcemia and hyperphosphatemia - decrease 1-alpha-hydroxylation of vitamin D by proximal renal tubule cells
Increased prolactin due to decreased prolactin excretion
Myoclonus
Osteomalacia
Elevated Anion gap metabolic acidosis
Uworld Step 2 says dialysis does not increase cancer risk
Management
Anemia: keep Hgb > 10 EPO, Iron
Secondary Hyperparathyroidism: use Cinacalcet (a calcimimetic) and phosphate binders ie sevelamer
Osteoporosis: Dexa > -2.5, use Ca, 1,25VitD
Volume Overload: Use loops then when that fails use loops + metolazone and if that fails --> Hemodialysis
Metabolic Acidosis: Keep Bicarb > 20, use NaBicarb
From best to worst for bleeding: correct anemia, desmopressin, dialysis, estrogen, cryoprecipitate
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Acute Interstitial Nephritis (Tubulointerstitial Nephritis)
Acute interstitial renal inflammation
Pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity
(Diuretics, penicillin derivatives (including cephalosporins), proton pump inhibitors, sulfonamides, rifampin, NSAIDs
Lead
Less commonly may be 2° to other processes
Systemic infections (eg, mycoplasma) or autoimmune diseases (eg, Sjögren syndrome, SLE, sarcoidosis)
Associated with fever, rash, hematuria, and costovertebral angle tenderness, but can be asymptomatic
Results in acute renal failure (intrarenal azotemia); oliguria; may become renal papillary necrosis
Increased levels of eosinophils and IgE
Edema and leukocyte infiltration of the interstitium
Considered both an IgE mediated hypersensitivty and IV hypersensitivity
WBC casts (WBC with Tamm-horsfall protein)
C. Proteinuria
Most commonly seen in females (peak at age 50-55 years, due to NSAID use)
+/- Arthralgias
Renal biopsy: Inflammatory infiltrate, edema
Less commonly, AIN may be caused by infectious agents (eg, Legionella, Mycobacteriurn tuberculosis , Streptococcus)
Management
Since it is a hypersensitivity, withdrawal of the drug will resolve it
+/- Systemic glucocorticoids
Pyelonenphritis and amyloidosis can be causes
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Acute Tubular Necrosis
Most common cause of acute kidney injury in hospitalized patients
Spontaneously resolves in many cases
Can be fatal, especially during initial oliguric phase
Necrotic cells plug tubules causing decrease in GFR
Increased FENa
Granular (“muddy brown”) casts (Pictured, A)
3 stages
Inciting event
Maintenance phase - oliguric; lasts 1–3 weeks; risk of hyperkalemia, metabolic acidosis, uremia
Increased creatinine/bun, fluid overload
Edema, pulmonary edema, weight gain, high anion gap metabolic acidosis
Often dialysis is used
Recovery phase—polyuric; BUN and serum creatinine fall; risk of hypokalemia
U. Less so but still important: hypophosphatemia and hypocalcemia; stage of re-epithelization
Renal colic may occur following sloughing of renal papilla
Ischemic cause
2° to decreased renal blood flow (eg, hypotension, shock, sepsis, hemorrhage, HF, acute MI, surgery etc.)
Results in death of tubular cells that may slough into tubular lumen (Pictured, B) (PCT and thick ascending limb are highly susceptible to injury)
For hypoxic causes not nephrotoxic causes!
Nephrotoxic cause
2° to injury resulting from toxic substances (eg, aminoglycosides, radiocontrast agents, lead, cisplatin), crush injury (myoglobinuria), hemoglobinuria
Ethylene glycol (oxalate crystals) and rate (e.g., tumor lysis syndrome)
PCT is particularly susceptible to injury; the renal medulla
Ischemic kidney can be a cause
Treatment: IV fluid prophylaxis (when the patient is given one of the toxins ie contrast, listed)
Administration of IV diuretics may be used as part of treatment
Tenofovir can be a cause
Bun/creatinine ratio: Typically normal (~10 -15)
Fractional excretion of sodium: >2%
Urine osmolality: ~300 mOsm/kg
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Renal Papillary Necrosis
Sloughing of necrotic renal papillae (Pictured)
Gross hematuria/proteinuria; flank pain
May be triggered by recent infection or immune stimulus
Associated with sickle cell disease or trait, acute pyelonephritis, NSAIDs, phenacetin, aspirin, diabetes mellitus, severe acute pyelonephritis
Urinary tract obstruction is also associated
White/yellow necrosis of the distal 2/3rds of the renal pyramids
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Diffuse Proliferative Glomerulonephritis
Nephritic
Most common form of renal disease in SLE
Due to SLE or membranoproliferative glomerulonephritis
LM—“wire looping” of capillaries
EM—subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
IF—granular
A common cause of death in SLE
DPGN and MPGN often present as nephrotic syndrome and nephritic syndrome concurrently
Proliferation/thickening (look at the name) of cells (lymphocytes and endothelium) within the capillary loops
U. Crescent formation during active part of disease
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Lung Development
Initial development includes development of lung bud from distal end of respiratory diverticulum during week 4
Lung bud divides into two bronchial buds that branch off into bronchi
Embryonic (weeks 4–7)
Lung bud Žto trachea Žto mainstem bronchi toŽ secondary (lobar) bronchi Žto tertiary (segmental) bronchi
Errors at this stage can lead to TE fistula
Pseudoglandular (weeks 5–16)
Endodermal tubules toŽ terminal bronchioles; Surrounded by modest capillary network
Respiration impossible, incompatible with life
Canalicular (weeks 16–26)
Terminal bronchioles Žto respiratory bronchioles toŽ alveolar ducts. Surrounded by prominent capillary network
Airways increase in diameter; Respiration capable at 25 weeks
Saccular (weeks 26–birth)
Alveolar ducts toŽ terminal sacs. Terminal sacs separated by 1° septae. Pneumocytes develop
Alveolar (weeks 32–8 years)
Terminal sacs toŽ adult alveoli (due to 2° septation)
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Hypersensitivity Pneumonitis
Mixed type III/IV hypersensitivity reaction to inhaled environmental antigen
Dyspnea on exertion, cough, chest tightness, headache, fever
Often seen in farmers and those exposed to birds "Pigeon breeder's lung"
Granulomatious reaction
Resolves with removal of antigen
Restrictive lung disease
Chronic exposure causes interstitial fibrosis
CD8+ predominance in lung lavage
Diffuse nodular x-ray
Also caused by molds associated with farming ("farmer's lung")
Clears up in a matter of one to two days so if someone leaves town (away from the antigen) they get better and then worse on arrival back
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