Ngs-ivy-pot Shared Oro - 74 Picmonics

Leuprolide

GnRH Agonist (Pulsatile Use)

GnRH Antagonist (Continuous Use)

Upregulates FSH And LH

Downregulates FSH And LH

Infertility

Prostate Cancer

Precocious Puberty

Uterine Fibroids

Endometriosis

Anti-androgenic Effects

2 mins

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 to acetylCoA + CO2 + NADH

Complex is similar to the α-ketoglutarate dehydrogenase complex (same cofactors, similar substrate and action), which converts α-ketoglutarate to succinyl-CoA (TCA cycle)

Arsenic inhibits lipoic acid. Findings: vomiting, rice-water stools, garlic breath

Thiamine pyrophosphate (B1 )

Lipoic acid

Lipoamide carries acyl groups

CoA (B5, pantothenic acid)

FAD (B2, riboflavin)

NAD (B3, niacin)

High NAD+/NADH ratio, ADP, Ca2+

Urea Cycle

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

Herniation Syndromes

Can compress anterior cerebral artery

Caudal displacement of brain stem causes rupture of paramedian basilar artery branches casuing Duret hemorrhages; Usually fatal

Hemorrhages occur in the pons and midbrain

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)

Coma and death result when these herniations compress the brain stem

Cardiopulmonary arrest

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

Aliskiren

Direct renin inhibitor

Blocks conversion of angiotensinogen to angiotensin I

Hypertension

Hyperkalemia

Decreased GFR

Hypotension

Relatively contraindicated in patients already taking ACE inhibitors or ARBs

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

Squamous Cell Carcinoma of the Bladder and Adenocarcinoma

Chronic irritation of urinary bladder causes squamous metaplasia leading to dysplasia and squamous cell carcinoma

Risk factors include Schistosoma haematobium infection (Middle East), chronic cystitis (older women), smoking, chronic nephrolithiasis

Presents with painless hematuria

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

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)

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

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)

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

Rare

Characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages

Grossly orange nodules that can mimic tumor nodules

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)

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

Decreased RBF (eg, hypotension or HF) decreases 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

Acute tubular necrosis or ischemia/toxin cause; less common acute glomerulonephritis (eg, RPGN, HUS) or acute interstitial nephritis

In ATN, patchy necrosis causing debris obstructing tubule and fluid backflow across necrotic tubule decreasing GFR

Urine has epithelial/brown granular casts

BUN reabsorption is impaired decreasing 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

Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies)

Develops only with bilateral obstruction

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)

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

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

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)

Since it is a hypersensitivity, withdrawal of the drug will resolve it

+/- Systemic glucocorticoids

Pyelonenphritis and amyloidosis can be causes

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)

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

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!

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

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

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

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

Lung bud to trachea to mainstem bronchi to secondary (lobar) bronchi to tertiary (segmental) bronchi

Errors at this stage can lead to TE fistula

Endodermal tubules to terminal bronchioles; Surrounded by modest capillary network

Respiration impossible, incompatible with life

Terminal bronchioles to respiratory bronchioles to alveolar ducts. Surrounded by prominent capillary network

Airways increase in diameter; Respiration capable at 25 weeks

Alveolar ducts to terminal sacs. Terminal sacs separated by 1° septae. Pneumocytes develop

Terminal sacs to adult alveoli (due to 2° septation)

Ngs-ivy-pot Shared "Oro" - 74 Picmonics

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