9 ⼀RENAL/UROLOGY/ID II Flashcards
239
What is Conn’s syndrome?
________________
dx?
Primary Hyperaldosteronism
2/2 excessive adrenal gland secretion ➜ polyuria and polydipsia
________________
[Plasma aldosterone : Plasma Renin ACTIVITY] > 30
What type of acid base disturbance does TB cause? Why?
TB is a common cause of Addison’s primary adrenal insufficiency which –> ⬇︎Aldosterone –> Normal Anion Gap Metabolic Acidosis
How is Allopurinol used to prevent kidney damage during CA tx?
Allopurinol prevents [tumor lysis-associated urate crystal nephropathy] in pts receiving tx for lymphoma/leukemia
Which drugs cause renal tubular obstruction and ➜ [Crystalline nephropathy Acute Tubular Necrosis]? - 5.0
“crystal MAPES obstruct kidneys!”
- MTX
- Acyclovir IV
- Protease inhibitors
- Ethylene glycol
- Sulfonamides
Uremia constitutes a BUN of ⬜
Name the classic s/s (3)
> 50
_________________
LAC
Lethargy | Anorexia & vomiting | Confusion
Why are DM pts who take SGLT2 inhibitors at ⇪ risk for DKA?
because [SGLT2 inhibitors] prevent Glucose reabsorption ➜ easier/faster for [fasting, exercise, abrupt insulin ∆] to activate ketogenesis = ketogenesis may occur in setting of [euglycemic DKA < 250 BG]
(normally: DKA is observed
Hemodialysis via tunneled catheter is a/w high rates of catheter-related bloodstream infxn
Typical management for catheter-related bloodstream infxn involves leaving tunneled Catheter in place and what else? (2)
_________________
When is immediate removal of [infected tunneled Catheter] indicated ? (5)
{Vancomycin + [cefepime|gentamicin]} ➜ [once afebrile, change catheter over guidewire]
_________________
Severe Sepsis | HDUS | pus at site | sx > 72h after abx | metastatic infxn
Demeclocycline MOA
blunts Collecting Duct resposne to ADH during SIADH ➜ water excretion
preferred over lithium which is similar
How do you determine if renal artery stenosis is the underlying cause of HTN in Kidney transplant patients?
_________________
explain
Give [ACEk2 inhibitor]. If Creatinine INC ➜ Renal Artery stenosis was the cause of HTN
_________________
(2/2 improper surgical anastomosis), renal artery stenosis (BL or solitary uL) causes DEC GFR and when [ACEk2 inhibitor] is given ➜ even lower DEC GFR. This very low GFR activates the renin-angiotensin-aldosterone system ➜ INC [Angiotensin 1 and 2] HAVDEN ➜ ultimately resistant hypertension, flash pulm edema
How do you workup hypOnatremia?
Patients with Chronic Kidney Disease develop ⬜ anemia that is treated with ⬜
Prior to giving this treatment, why must iron be assessed first?
normocytic; Erythropoietin
_________________
[EPO ➜ vigorous hematopoiesis ➜ rapid depletion of iron stores ➜ IDAfn]
so MD must ensure iron stores are sufficienct prior to giving EPO
Erythrocytosis in patients with hematuria and smoking hx should always make you think of (and rule out) ⬜
RCC (HAWF) = GET CT abd!
_________________
RCC ➜ Erythropoietin secretion ➜ Erythrocytosis
HAWF= Hematuria/Abd mass/Wt loss/Flank Pain
⬜ is the most common cause of nephrOtic syndrome in kids and presents with ⬜
_________________
Tx?
Minimal change disease; [CLag]
_________________
CTS
_________________
[CLag = ⇪ Coagulation/Lipidemia /⬇︎albumin/gammaglobulin]
rapid remission with CTS but has HIGH relapse rate = frequent UA
Both AiN and Pyelonephritis involve intrusion of the tubulointerstitium. What’s the major difference?
[AiN = mononuclear cell]
vs
[Pyelonephritis = neutroPhil]
[AiN] MOD
[RiPAN –mo–> FAPES]
hypersensitivity to [RiPAN antigen] ➜ moNONUCLEAR CELLS infiltrating tubulointerstitium➜ FAPES
_________________
RiPAN = Rheum/iNfection/PPI/Abx/NSAIDs
FAPES = FEVER / AKI intrarenal / [Pyuria +/- WBC cast] / [Eosinophilia (blood +/- urine)] / Skin rash]
[AiN] sx (5)
FAPES = FEVER / AKI intrarenal / [Pyuria_sterile+/- WBC cast] / [Eosinophilia (in blood +/- urine)] / [Skin rash]
_________________
[RiPAN –mo–> FAPES]
RiPAN = Rheum/iNfection/PPI/Abx/NSAIDs
ATN MOD
[⬇︎renal perfusion] ➜ [Acute Tubular Necrosis of tubular epithelium] ➜ sloughing of necrotic medullary cells ➜ [mBGC and/or rTEC/C]
w
[💢flank]+/- hematuria (more common in GN)
💢= pain
🔎mBGC = muddy Brown Granular cast
🔎rTEC/C = renal Tubular Epithelial Cell/cast
clinical presentation of [radioContrast associated AKI]
24-48h after contrast ➜ = [contrast induced nephropathy] = nonoliguric intrarenal AKI⼀ATN⼀mBGC
🔎mBGC = muddy Brown Granular Cast
How do you determine cause of an AKI? -4
PHEOCHromocytoma
clinical features (6)
PHEOCHromocytoma
Palpitations
HA
Episodic SWEATING
Orthostatic hypOtension
([Catecholamine & Metanephrine 24h urine] or [free plasma metanephrine] = dx)
HTNrefractory
a patient with positive labs for PHEOCHromocytoma has negative imaging results
What’s the next diagnostic used?
_________________
When can surgical removal occur?
[MIBG scan]
_________________
Adrenalectomy only after [10 day preOp BP control with αB➜ (+ BB)]
_________________
MIBG = MetaIodoBenzylGuanidine (resembles NorEpi ➜ will be taken up by rogue adrenergic tissue = locates tumors not seen by imaging) // [αB = α R Blocker]
PHEOCHromocytoma patients undergoing adrenalectomy may experience hypOtension and HYPERtension intraoperatively
How is [PHEOCHromocytoma-related_hypOtension] treated?
_________________
[PHEOCHromocytoma-related_HTN] treated?
PHhypOtension ➜ [NS IV bolus]
_________________
PHHYPERtension ➜ give [phentolamineα1🟥 IV bolus]
_________________
Dopamine/Dobutamine can’t be used in PHEOCHromocytoma hypOtension 2/2 chronic α R Blockade
clinical features of BrIAn (3)
_________________
Berger IgA nephropathy
- [URI ➜ Recurrent GROSS hematuriia]
- [NORMAL COMPLEMENT (PSGN-PiG = low complement)]
- [POOR PROGNOSIS if Cr ⇪ / BP ⇪ / persistent prOteinuria]*
_________________
*BP>140/90 / [pp> 1 gm per day]
Why is rapidly worsening kidney function (⬇︎GFR or ⇪[urine albumin/Cr ratio]) highly concerning for Diabetic Kidney Disease?
Diabetic Kidney Disease is a SLOW PROGRESSIVE KIDNEY DETERIORATION.
Rapid Deterioration suggest ANOTHER ETX➜ WARRANTS RENAL BIOPSY
Dx for Rhabdomyolysis (2)
[⊕gross blood on UA](2/2 [hgb lab test’s] cross reactivity with myoglobin)
but
[⊝RBC actually seen on Umicro](indicates ⊕UA likely from presence of myoglobinwhich → rhabdomyolysis dx)
rhabdoM dx= {[⊕blood_UA] but [⊝RBC_UMicro]}
[Mixed Cryoglobulinemia Syndrome] etx
_________________
How is it diagnosed?
[(most common: chronic HepC) vasculitis] that involves [polyclonal IgG and (Rheumatoid Factor IgM)] depositing in vascular walls of small & medium vessels ➜ [PAW-CPR-GNC]
_________________
dx = ⇪ serum cryoglobulins
MIXED PCG!
[Mixed Cryoglobulinemia Syndrome] etx
_________________
How do you treat Mixed Cryoglobulinemia Syndrome ? (2)
[(most common: chronic HepC) vasculitis] that involves [polyclonal IgG and (Rheumatoid Factor IgM)] depositing in vascular walls of small & medium vessels ➜ [PAW-CPR-GNC]
_________________
MIXED PCG!
Tx = [Immunosuppressants (CTS/rituximab)] ➜ [treat underlying cause (common HepC]
[Mixed Cryoglobulinemia Syndrome] etx
Mixed = [Type 2 vs Type 3] = [(chronic HepC > chronic HBV|autoiummune) ] –> [B cell hyperactivation] –> {mixed [polyclonal IgG and (Rheumatoid Factor IgM)] Immune Complex} depositing in small & medium vasc walls ➜ [PAW-CPR-GNC]
_________________
sx: MIXED PCG!
[Mixed Cryoglobulinemia Syndrome]
Name the clinical features (9)?
MIXED PCG!
PAW CPR GNC
Palpable purpura **
Arthralgias **
Weakness Fatigue **
Complement is low
Peripheral neuropathy
[Rheumatoid factor IgM elevated]
[Glomerulonephritis (RBC cast, RBC, prOteinuria)]
Nausea
Chronic HCV
⬜ is an important cause of secondary HTN in adults < 30 yo. How is this a/w Glomerulonephritis?
[Renal parenchymal disease] ; Glomerulonephritis (nephritic or nephrOtic) can ➜ secondary HTN because of INC renal Na+ reabsorption
telltale clinical sign of Rhabdomyolysis
[⊕gross blood on UA]
but also has
[⊝/min actual RBC on UMicro]
= (indicates myoglobinuria instead of hgburia)
rhabdoM dx= {[⊕gross🩸UA] but [⊝RBCUMicro]}
etx of Rhabdomyolysis?
MUSCLE INJURY ➜ release of intracell components of muscle cell ([CPK > 10K] & [myoglobin ➜ AKI])
tx = aggressive IVF to prevent intratubular cast formation
rhabdoM dx= {[⊕blood_UA] but [⊝RBC_UMicro]}
What is Orthostatic prOteinuria? (2)
_________________
How is it diagnosed?
- [OAIP- Orthostatic adolescent isolated prOteinuria] = most common cause of teenage prOteinuria
- exaggerated [angiotensin II] response to upright posture (especially during day when pt stands more) ➜ ⇪ GFR ➜ prOteinuria
_________________
[Split 24H urine collection (12H Day + 12H Night)] ⼀demonstrating elevated prOteinuria during Day but normal at night ]
OAIP treatment?
Orthostatic Adolescent isolated PrOteinuria
NOTHING!
self limited with age
Both concentric LVH and Eccentric LVH are common in CKD
Explain why for each
▶poor volume regulation ➜ pressure overload ➜ Chronic Systemic HTN ➜ concentric LVH
▶CKD ➜ anemia ➜ myocardial hypoxia/necrosis/fibrosis ➜ compensatory remodeling ➜ Eccentric LVH
Erythropoiesis Stimulating Agents (such as ⬜2) are used to treat ⬜
▶When is it beneficial to give ESA to these patients?
▶▶ Name the benefits (3)
Epoetin | darbEpoetin ; [CKD's severe anemia hgb\<10]
▶ hgb\<10
Erythropoiesis Stimulating Agents (such as ⬜2) are used to treat ⬜
▶When is it Risky to give ESA to these patients?
▶▶ Name the potential Risk (3)
Epoetin | darbEpoetin ; [CKD's severe anemia hgb\<10]
▶ hgb\>13
Erythropoiesis Stimulating Agents (such as ⬜2) are used to treat ⬜
How do you manage Anemia 2/2 Chronic Kidney Disease?
Epoetin | darbEpoetin ; [CKD’s severe anemia hgb<10]
_________________
Treatment of [CKD’s severe anemia hgb<10] with [Erythropoiesis Stimulating Agents] improves ⬜ and reduces ⬜
QOL
LVH
What are the common precipitants of SIADH? (11)
- Neuro (stroke, hemorrhage, trauma)
- Lung (PNA, SOLC)
- Somatic (Pain, Nausea)
- Meds (SSRI, Carbamazepine, Valproate, NSAIDs)
_________________
tx = [fluid restriction +/- salt tablets]
What is one of the telltale signs of analgesic induced nephropathy?
ACUTE SEVERE PROTEINURIA on AiN_AKI
_________________
NSAIDs inhibit prostaglandin production (prostaglandins preferentially vasoDilate Afferent arteriole ➜ ⇪ GFR) = [NSAIDs ultimately➜ DEC GFR] and NSAIDs directly cause AiN
⬜ is a telltale sign of analgesic induced nephropathy
How does NSAIDs actually cause Renal damage? (2)
ACUTE SEVERE PROTEINURIA on AKI
_________________
▶NSAIDs inhibit prostaglandin production (prostaglandins preferentially vasoDilate Afferent arteriole ➜ ⇪ GFR) = [NSAIDs DEC GFR]👎🏾
▶▶NSAIDs also directly cause AiN
What are the 4 major complications of any NephrOtic syndrome
CLag
- ⬆︎Coagulation from loss of AT3 (MOST COMMON WITH MEMBRANOUS NEPHROPATHY)
- ⬆︎Lipidemia –>loss of lipoproteins = [Fat oval body Maltese crosses] in urine
- ⬇︎albumin
- ⬇︎gammaglobins –> infection
Why are pts with nephrotic syndrome at increased risk for accelerated Atherosclerosis?
CLag
⬆︎Lipidemia from loss of lipoproteins
5 main serum electrolyte changes due to Chronic Kidney Dz
- ⬆︎ K+
- ⬆︎Mg
- ⬆︎H+
- ⬆︎ Phosphate
________________
- DEC Ca+
What agents induce Renal dysfunction via Afferent Arteriole vasoconstriction-5
NARCO
- NSAIDs
- Amphotericin B
- Radiocontrast (also causes oxidant injury)
- Cyclosporine
- tacrOlimus
Identify the type of cast and associated Disease
[muddy Brown Granular Cast] = Acute Tubular Necrosis
Identify the type of cast and associated Disease
RBC Cast = [Acute Glomerulonephritis_nephritic]
Identify the type of cast
________________
what 2 Disease is it associated with?
WBC Cast =
AiN (Acute allergic interstitial nephritis)
or Pyelonephritis
UA for Acute Tubular Necrosis - 3
- [mBGCmuddy Brown Granular Cast]
- [RTEC/C (Renal Tubular epithelial cells/cast)]
- Hematuria
UA for AiN (2)
(Acute allergic interstitial Nephritis)
[Sterile WBC Pyuria]
plus
[EosinophilicWBC Cast]
UA for
[Acute Glomerulonephritis nephritic syndrome] -3
- [Hematuria dysmorphic RBCs]
- Proteinuria
- [RBC Cast]
_________________
These pts will also have HTN
What type of cast are seen in [Acute Glomerulonephritis nephrOtic syndrome]? (3)
- [Hematuria dysmorphic RBCs]
- Proteinuria
- [Fatty OvalBody cast]
What type of cast are seen in Chronic Renal Failure?
Waxy broad cast
Why does Chronic Kidney Disease cause anemia? (4)
- DEC renal EPO
- [IDAfn 2/2 ACD] ⼀ [Chronic Disease (CKD)]➜ inflammation ➜ INC hepcidin ➜ prevents macrophages from releasing iron into plasma ➜ iron sequestration = [inadequate iron stores (low ferriTin)] due to ACD
- [IDAfn 2/2 ESA mismatch] ⼀occurs when, despite nml iron stores, there’s still not enough iron to keep up with the accelerated erythropoiesis from ESA
- Uremia ⼀➜ DEC RBC lifespan
_________________
[IDAfunctional (nml ferriTin)] / [IDAABSOLUTE (low ferriTin)] / ESA=Erythropoietin Stimulating Agent
What is the potential long term effect of donating your kidney?
Gestational complications
_________________
(preeclampsia, gestational DM, gestational HTN) = women should complete child bearing prior to donating kidney
MOD for [PSGN PiG]
_________________
PostStreptococcal GlomeruloNephritis PostInfectious Glomerulonephritis
1-2 weeks after [Strep or Staph infection] immune complex deposit in the [glomerular Basement Membrane subepithelium] ➜ permitting protein and RBC to cross into urine= [AGN nephritic] ➜ prOteinuria→ edema, HTN and hematuria→ RBC cast
Early diabetic Kidney Disease is characterized by ⬜
Explain MOD
glomerular hyperfiltration
_________________
DM-related hormonal mediators cause renal afferent vasoDilation and efferent vasoconstriction ➜ [⇪ GFR(glomerular hyperfiltration)] –(over time)–> glomerular sclerosis = Diabetic Kidney Disease
ACEk2 inhibitors and ARBS ⬇︎Angiotensin (which normally vasoconstricts efferent arteriole) ➜ efferent arteriole vasoDilation ➜ ⬇︎ GFR and prevents DKD
How do you manage an obstructive ureteral stone (ureterolithiasis) that’s causing hydronephrosis? -2
DECOMPRESS UPPER URINARY TRACT BY DRAINING THE HYDRONEPHROSIS (proximal to the ureteral stone ) via Percutaneous Nephrostomy > retrograde ureteral stent
_________________
any [complicated ureterolithiasis] = a/w infxn, AKI, severe pain, hydronephrosis or failed initial tx] ➜ [Proximal Ureteral Decompression by PQ Nephrostomy]
list the main features of Shock-wave lithotripsy (3)
- indicated for UNCOMPLICATED proximal ureteral stones
- does not immediately relieve obstruction
- = complicated ureterolithiasis (unstable/infection/AKI) must first have [Proximal Ureteral Decompression via PQ nephrostomy] before having Shock wave Lithotripsy
⬜ such as Tamsulosin have been shown to facilitate Kidney stone passage with stones size ⬜
[ α1🟥 ] ; [small < 10 umm]
Clostridioides Difficile
Recite the 4 *SYMPTOM GRADES* for CDiff \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
What are the 2 treatment regimens?
(see image)
Clostridioides Difficile Infection
GRADE 1 = initial presentation = CDITxA
1. [Cdiff ⊕stool test +/- RF]
2. [ Diarrhea WATERY x ≥3 per day]
3. [ Intestinal abdP]
GRADE 2 = severe CDITxA
GRADE 3 = Fulminant CDITxA
GRADE 4 = REFRACTORY CDITxB
_________________
TxA = {[(fidaXomicin PO10d) or (Vancomycin PO10d)] –if fail–> (PO metro)}
TxB: [fecal microbiota transplant | Surgery]
_________________
🔎abdP = abdominal Pain
chronic Giardia cp (2)
_________________
Tx? (2)
-watery diarrhea
-[weight loss (2/2 malabsorption)]
_________________
Tinidazole (or nitaZoxanide)
non-inflammatory diarrhea = negative fecal leukocytes
Tx options for Cellulitis -6
Cellulitis Can Be Decreased Via PipTazo
- Clindamycin **
- Cephalexin
- Bactrim
- Doxy
- Vancomycin
- [Piperacillin/Tazobactam (PipTazo)]
List the best abx options for aspiration PNA - 3
foul sputum, fever, cough
- CLINDAMYCIN
- [amox/clav]
- [amox/metronidazole]
What disease should you suspect in a [DM pt with DKA who’s just developed a fever, nasal congestion, HA and sinus pain]?
[ROC mucormycosis]
_________________
ROC: Rhino-Orbital-Cerebral
[ROC Mucormycosis] is mostly seen in patients with ⬜.
Treatment includes ⬜2
_________________
ROC: Rhino-Orbital-Cerebral
DKA
_________________
[(Amphotericin BLiposomal IV) + surgical debridement]
uncontrolled HIV+ patient with [widespread papules containing central umbilication and central hemorrhagic necrosis] suggest ⬜
cryptococcus neoformans cutaneous
_________________
USUALLY IN CD4 < 100 AND IS MARKER OF DISSEMINATED DISEASE
Immunocompromised patient with ⬜(description) skin lesions has just been diagnosed with [Cryptococcus Neoformans ⼀cutaneous]
_________________
How is this diagnosed?
[widespread papules containing central umbilication & central hemorrhagic necrosis]
_________________
[BIOPSY of lesion revealing hyperplasia of dermis overlying granulomas with encapsulated yeast]
⬜ (caused by ⬜) is the leading cause of Dilated Cardiomyopathy in Central/South America
_________________
⬜ is the main Sx, but what are the other 5 sx?
[Chagas Heart Disease] ; [Trypanosoma Cruzi protozoa]
_________________
[L Vt apical aneurysm] in the absence of coronary disease
2) [HF (R>L)]
3) Mural thrombosis
4) [Conduction ∆ 2/2 fibrosis (complete heart block/VT)]
5) Dilation of Esophagus
6) Dilation of Colon
What are the guidelines regarding [Active TB infection] and Healthcare Personnel who’ve been exposed? (5)
- [Active TB infection] can transmit Mycobacterium Tuberculosis to close contacts starting 3 mo before sx onset = Healthcare Personnel are at risk!
- exposed HCP should receive [TST or IGA] screening
- –(if negative)–> Repeat [TST or IGA] in 8 weeks
- –(if positive)–> [CXR and Sx review] to determine ATBI or LTBI.
5.- ATBI = confirm with sputum mycobacterial acid-fast if + ➜ ATBI tx
if *neg ➜ LTBI tx
Diagnostic criteria for [LTBI (Latent TB Infection)] -3
[⊕ TST/IGA]
[NO sx(cough>3mo, wt loss, night sweats, fever)]
[NO CXR findings(cavitation/infiltrate)]
________________
determine LTBI tx using susceptibility from the initial TB source
Diagnostic criteria for ACTIVE PULMONARY TB -3
[⊕ TST/IGA]
PLUS
[⊕TBSx (cough>3 mo, wt loss, night sweats, fever)]
and/or
[⊕ CXR (cavitation/infiltrate)]
What is the treatment regimen for ACTIVE PULMONARY TB -2
________________
+TST/IGA with [+CXR and/or +TBSx]
[RIPE]2 ➜ [RI]4
________________
RIPE = Rifampin/Isoniazid/Pyrazinamide/Ethambutol
tx for [LTBI (Latent TB Infection)] -4
1st line: [( Ri ) qd]3
________________
- 3 LTBI tx Alternatives: (see image)*
- determine LTBI tx using susceptibility from the initial TB source*
What is the treatment for ACTIVE TB in pregnant patients? (3)
( [RIE2 ➜ RI7] + [Pyridoxine B6] )
_________________
3-DRUG THERAPY (RIPE)
- [2 mo RIE”Ree2”] ➜ [7 mo RI”Ry7”]*
- pregnant women with ACTIVE TB should be treated*
Normally, positive TST = induration ⬜ mm
Which patients only need > 5 mm induration to be considered positive TST? (5)
_________________
TST = Tuberculin Skin Test
> >15 mm
_________________
pts below only require > 5 mm induration:
1. HIV⊕
2. Transplant recipient⊕
3. Immunocompro
4. [⊕ Recent TB exposure]
5. [⊕CXR showing fibrotic ∆ c/f TB]
Normally, positive TST = induration ⬜ mm
Which patients only need > 10 mm induration to be considered positive TST? (4)
_________________
TST = Tuberculin Skin Test
> >15 mm
_________________
pts below only require > 10mm induration:
1. [kids < 4 yo]
2. [HIGH RISKpersonnel healthcare|jail|homeless shelter]
3. [recent immigrant from TB_country]
4. IVDA
Normally, positive TST = induration ⬜mm after ⬜hours
_________________
What does
[⊕(TST or IGA)]
with
[⊝(CXR or TB sx)] indicate?
>15 mm ; 48h
_________________
⊕LTBI
⊕[Latent TB infection] = pt has been exposed to TB sometime in the past and was never treated ➜ (non-infectious) [Latent “dormant” TB infection]
STI screening depends on gender, sex orientation, behavior
Especially in ages 13-75, which STI should you routinely screen for regardless of sexual risk factors?
HIV
_________________
[HIV p24 antigen] and [HIV-1 / 2 Ab screen]
tx for Mycobacterium Avium Complex-3
REC the MAC
Rifambutin
Ethambutol
Clarithromycin
Which organisms usually cause UTI-associated Sepsis?-4
KEEP away, UTI!
Klebsiella
E.Coli
EnteroCoCCus
Proteus
Why are pts Suspected of bacterial meningitis placed on ⬜ precaution?
Droplet precaution
_________________
UNTIL NEISSERIA MENINGITIDIS IS RULED OUT!
“BANGIR needs to drop what he’s doing and don a basic facemask, right now!”
empiric Tx for Meningitis in pts [<1 months] (4)
B-E-Lag |a🅇
_________________
[Amp/Gent(any aminoglycoside)] or
[Amp/cefoTA🅇ime]
DDx for Meningitis in pts [<1 months] (3)
B-E-L
ag|a🅇
[Amp/Gent(any aminoglycoside)] or
[Amp/cefoTA🅇ime]
empiric Tx for Meningitis in pts [1 mo- 23 mo] (2)
B-E-H-N-SVX
_________________
[Vanc + (CefTriaXone | cefoTaXime)]
DDx for Meningitis in pts [1 mo- 23 mo] (5)
B-E-Hflu-N-SVX
empiric Tx for Meningitis in pts [2 yo - 50 yo] (2)
H-N-SVX
_________________
[Vanc + (CefTriaXone | cefoTaXime)]
DDx for Meningitis in pts [2 yo - 50 yo] (3)
HSV-N-SVX
empiric Tx for Meningitis in pts [>50 yo] (4)
A-N-S-LVAXS
_________________
Vanc
+ Ampicillin
+ [(CefTriaXone | cefoTaXime))]
+ [Steroids CTS](Dexamethasone) ⬇︎ hearing loss and death a/w Strep Pneumo
DDx for Meningitis in pts [>50 yo] (4)
A-N-S-LVAXS
ALL DM pts require [Diabetic Kidney Disease] screening every ⬜ with ⬜.
Normal urine albumin excretion is ⬜.
[⬜ = moderately INC albuminuria] and [⬜ = severely INC albuminuria]
[year ([DM1: starts 5y after dx] / [DM2: starts 1y after dx])]
[Urine a/c ratio]
_________________
[<30 mg/day] ;
[30-300 mg/day] ; [>300 mg/day]
a/c: albumin/creatinine
Opioids are dangerous for pts with Kidney dysfunction
Why is giving morphine to pts with Kidney dysfunction even more dangerous than if giving any other opioid? (2)
> a. Morphine undergoes 2-step metabolism–1st: catabolism into {m3G and [m6G(MORE POTENT)]}2nd: both kidney excretion
b. Kidney dysfunction→ DEC kidney excretion → accumulated m6G→ [INC risk OPIOID TOXICITY/OD (especially if postop)]
* * *
* m6G: [morphine-6-glucuronide]*
[exogenous EPO abuse (AKA doping)]
▶ ⬜ hematocrit
▶can be detected via ⬜
▶causes what 2 potential complications?
INC; [urine recombinant EPO];
- Hyperviscosity (HA, visual ∆ )
- Thrombosis (MI, CVA/TIA)
How are staghorn calculus formed? (3)
▶[Proteus mirabilis and Klebsiella Pneumoniae] produce Urease which hydrolyzes [urea → Ammonia]
▶▶[Ammonia alkalinizes urine pH>8] → precipitates crystallized [MAPS kidney stones]
▶▶▶ MAPS exposed to lrge amounts urea rapidly expand → [STAGHORN CALCULUS (*also seen with uric acid & cysteine kidney stones)]
_________________
MAPS: Magnesium Ammonium Phosphate Struvite
What is a staghorn calculus?
tx? (2)
[MAPSLARGE KIDNEY STONE] that fills entire renal pelvis → unable to pass in ureter = [severe colicky flank pain + fever + dysuria]
COMPLETE REMOVAL + abx
_________________
MAPS: Magnesium Ammonium Phosphate Struvite
- Describe how Kidney Stone size determines management
- and list the medical mgmt for Kidney stones (4)
[spontaneous ← 4mm–(Rx PASS)–10mm →Surgical]
Rx = [Pain control, {Alpha R blockers}4w, Strain urine, Solvent(IV Hydration)]
Kidney Stone size determines management
When all should you consult surgical (Urology) mgmt? (5)
a. ≥10mm
b. uncontrolled pain
c. ⊕AKI
d. ⊕UTI
e. [no stone passage in 4-6 wks]
Patient presents for Kidney Stone with symptoms
How do you manage this?
Pt pmhx BPH, lumbago s/p Baclofen for pain, p/w suprapubic fullness and discomfort
What is the Diagnosis?
Management?
▶Acute Urinary Retention 2/2 [bladder outlet obstruction (INC Risk with [Rx: baclofen/anticholinergics], GU trauma, UTI)](dx confirmed via bladder US > 300cc)
▶Bladder decompression [Catheterization (URETHRAL(if no GU trauma) → suprapubic(if urethral unsuccessful))]
pts with ⬜ have INC risk for [ROC mucormycosis], and usually presents with what sx? (5)
⼀
ROC : Rhino-Orbital-Cerebral
[DKA(likely 2/2 poorly controlled DM)] ;
rapid…
- nasal necrosis
- facial swelling
- fever
- HA
- sinusitis
rhino-orbital-cerebral
How does Calcium travel in the blood? (3)
and How does this affect lab interpretation in patients with Liver Failure?
[ALBUMIN-Ca+]45% > [FREE ionized Ca+]40% > [anion(O&iO)-Ca+]15%
_________________
serum Ca+ concentration DEC by 0.8 for every DEC of 1 by Albumin =
{[Albumin ⬇︎ 1] = [Ca+ ⬇︎0.8]}
- [O&iO: Organic&inOrganic] | [Albumin]g/dL | [Calcium]mg/dL*
Name the 7 dietary interventions (and their mechanism of action) for preventing CalciumCa +Phosphate | Ca+Oxalate Kidney Stones
“⇪Fluids Plus Citrate|⼀Can⼀ | ⬇︎Overall Agonizing Stones*| 💊r Take Pills”
🍴(⇪ FPC 🄲 ⬇︎OAS )🆚 💊TP
_________________
_________________
⇪ [Fluids > 2L urine/day](INC urine flow/DEC urine concentration)
⇪ [Potassiumcitrateavailable via🍌and💊!](INC urinary Citrate → binds urinary Ca+ → DEC Ca+ kidney stone formation)
⇪ [Citrate fruits/vegetables](binds urinary Ca+ → DEC Ca+ kidney stone formation)
__ __ __
(maintain)⼀ [dietaryCalcium intake 1200 mg/day]([GI dietary Ca+] binds [GI dietary Oxalate] → DEC reabsorption of [GI dietary Oxalate] → [DEC renal Oxalate] available → {[DECREASED [Ca+♉XALATE (only!)] kidney stone formation} )
__ __ __
⬇︎ [dietary (Spinach)Oxalate]DEC reabsorption of [GI dietary Oxalate] → [DEC renal Oxalate] available → {[DECREASED [Ca+♉XALATE (only!)] kidney stone formation} )</sup>
⬇︎[Animal protein](DEC renalCa+ excretion)
⬇︎[Sodium < 2300 mg/day](→ INC renalCa+ reabsorption → DEC urinaryCa+ available → DEC Ca+ kidney stone formation)
_________________
_________________
♉= DEC [Ca+♉XALATE] *kidney stone formation* only!
All other methods apply to both [Ca+_Phosphate and Ca+_Oxalate stones]
Name the 2 pharmacologic interventions (and their mechanism of action) for preventing Calcium Kidney Stones
- [ThiazideINC renal Ca+ reabsorption → DEC urinary Ca+ available →DEC Ca+ kidney stone formation]
- [Potassiumcitrateavailable via🍌and💊!](INC urinary Citrate → binds urinary Ca+ → DEC Ca+ kidney stone formation)]
_________________
“⇪Fluids Plus Citrate|⼀Can⼀ | ⬇︎Overall Agonizing Stones</sub>| 💊rTake Pills”
( ⇪FPC 🄲 ⬇︎OAS)🆚 TP
[PSGN-PiG] is a complication of (and presents 1-4 weeks after..) ⬜. It presents as a [⬜ nephritic | nephrOtic] syndrome]
_________________
Name the [PSGN-PiG] Laboratory Findings UA-3 vs Serum-5
[GASP > Staph infxn]; nephriiiitic
_________________
_________________
UA🟡:
🔬 prOteinuria
🔬[RBC dysmorphic]hematuriiia,
🔬[RBC cast]hematuriiiia
_________________
Serum🔴:
🔬⇪Creatinine
🔬⬇︎C3 complement
🔬[↧C4 complementnormal or low]
🔬⬇︎CH50 complement
🔬[⊕STREPTOZYME4= (∀streptolysinO 🆚 ∀DNAseB 🆚 ∀hyaluronidase 🆚 ∀streptokinase)]
🔎 ∀= [Anti___]
🧠PSGN-PiG etx: 1-4 weeks s/p [GASP>Staph] immune complex(Ig+antigen+[C3, C4, CH50]) deposit in GBMsubEpi] ( with pgn inverse to age)➜
1. [AGN AKInephritic]→ 🔬⇪ Creatinine, [🔬⬇︎C3, 🔬↧C4, 🔬⬇︎CH50 ], 🔬⊕STREPTOZYME4 = [💊Hemodialysis prn refractory, [💊supportive]
2. [🔬prOteinuria UA]→ edema, volume overload, HTN = [💊diuretics], [💊antiHTN]
3. [hematuriiia cola-urine🔬RBC dysmorphic UA and 🔬RBC Cast UA</sup]
[PSGN-PiG]
Treatment (4)
🧠PSGN-PiG etx: 1-4 weeks s/p [GASP>Staph] immune complex(Ig+antigen+[C3, C4, CH50]) deposit in GBMsubEpi] ( with pgn inverse to age)➜
1. [AGN AKInephritic]→ 🔬⇪ Creatinine, [🔬⬇︎C3, 🔬↧C4, 🔬⬇︎CH50 ], 🔬⊕STREPTOZYME4 = [💊Hemodialysis prn refractory, [💊supportive]
2. [🔬prOteinuria UA]→ edema, volume overload, HTN = [💊diuretics], [💊antiHTN]
3. [hematuriiia cola-urine🔬RBC dysmorphic UA and 🔬RBC Cast UA</sup]
[PSGN-PiG] is a complication of (and presents 1-4 weeks after..) ⬜. It presents as [⬜ syndrome] and is most common in ⬜.
Young Kids recover from [PSGN-Pig] in weeks = Good PGN. Adults do NOT.
What Adult demographics have Poor [PSGN-PiG] Prognosis (develops ESRD) ? (4)
initial[GASP infection]; [nephritic (AKI, prOteinuria/edema/volumeOverload/HTN, hematuriiia/RBC/RBC cast/cola urine)]
- 40% Adults in general
- CKD Adults
- [Metabolic Syndrome X] Adults
- DM Adults
Pt p/w cola-colored urine after exercise
Despite being ⬜ , [Exercise-Induced Hematuria] is 1 of 3 DDx for [hematuria after exercise]
◭What’s the pathophysiology for [Exercise-Induced Hematuria] ? (2)
◮management?
_________________
Name the other 2 DDx
diagnosis of exclusion;
[hematuria after exercise] DDx:
1. [ExerciseContact&NonContact-induced hematuria] =
A. [bladder jarring: repetitive up/down mvmt or trauma to bladder +
B. [kidney shunting:* exercise shunting of blood away from visceral organs like kidney**]→ hematuria*
- = **1 week follow up to confirm [self-limited spontaneous hematuria resolution] on repeat UA*
- *
2. [myoglobinuria 2/2 rhabdomyolysis]
3. [March hgburia 2/2 RBC trauma]
- *
_________________
C & NC: Contact & NonContact
(acute HCV) infection frequently presents as ⬜ but may also present with ⬜3.
How is (acute HCV) dx confirmed?
**ASYMPTOMATIC**
2. malaise
3. nausea
4. [RUQ pain with transaminitis]
* * *
* acute HCV:* [**⊕HCV<sub>RNA PCR</sub>**→ ⊕antiHCV ab within 12w]
(acute HCV) infection frequently presents as ⬜ but may also present with ⬜3.
How is (Chronic resolved HCV) dx confirmed? (3)
**ASYMPTOMATIC**
2. malaise
3. nausea
4. [RUQ pain with transaminitis]
* * *
* CHRONIC RESOLVED HCV:*
[⊕<sub>anti</sub>HCV ab]
[**NEG** HCV<sub>RNA PCR</sub>]
[**NEG** transaminase]
Rabies is a ⬜ primarily acquired via ⬜
[T or F] :[postexposure Rabies Prophylaxis] can prevent development of Rabies infection
fatal virus ; [rabid animal’s bite/scratch’s saliva]
_________________
TRUE
[viP(O)RIC] can prevent development of Rabies infection
**[V-i-P-(O)-RIC] [(VARID/ipris) Prophylaxis pOst-exposure Rhabdovirus Immunization Course)]
Rabies is a ⬜ primarily acquired via ⬜
What is the prescription for preexposure Rabies prophylaxis?
fatal virus ; [rabid animal’s bite/scratch’s saliva]
[viP(e)RIC] =
[VARID]4X
**[V-i-P-(e)-RIC] [(VARID/ipris) Prophylaxis prE-exposure Rhabdovirus Immunization Course)]
[(VARID) Vaccine ⼀ACTIVE RABIES IMMUNIZATION (Delayed-Ab)] → virus-neutralizing Ab Delayed available within 10d
K4X = 4 doses of
Rabies is a ⬜ primarily acquired via ⬜
What is the prescription for postexposure Rabies prophylaxis? -2
fatal virus ; [rabid animal’s bite/scratch’s saliva]
[viP(O)RIC] can prevent development of Rabies infection =
{[VARID4X + ipris1X] <-N- [PREVIOUS RABIES VACCINE?] -Y-> [VARID2X]}
**[v-i-P-(O)-RIC] [(VARID/ipris) Prophylaxis pOst-exposure Rhabdovirus Immunization Course)]
[(VARID) Vaccine ⼀ACTIVE RABIES IMMUNIZATION (Delayed-Ab)] → virus-neutralizing Ab Delayed available within 10d
[(ipris) Ig ⼀passive rabies immunization (STAT-Ab )] → virus-neutralizing Ab STAT IMMEDIATELY AVAILABLE
K4X = 4 doses of
In addition to [Rabies Physical Prophylaxis(⬜ wound cleaning)],
the 2 types of [Rabies Chemical Prophylaxis (⬜ and ⬜)] are
used in the [⬜ Regimen for preexposure Rabies Prophylaxis] and [⬜ Regimen for postexposure Rabies Prophylaxis]
RPP
[povidone⼀iodine]
RCP
[(VARID)] ; [(ipris)]
regimens:
viP(e)RIC ; viP(O)RIC
Rabies is a ⬜ primarily acquired via ⬜
In addition to [Rabies Physical Prophylaxis(⬜ wound cleaning)],
the 2 types of [Rabies Chemical Prophylaxis]
Describe the 2 types of [Rabies Chemical Prophylaxis]
fatal virus ; [rabid animal’s bite/scratch’s saliva]
[povidone⼀iodine]
[(VARID) Vaccine ⼀ACTIVE RABIES IMMUNIZATION (Delayed_Ab)] → virus-neutralizing Ab Delayed available within 10d
[(ipris) Ig ⼀passive rabies immunization (STAT_Ab )] → virus-neutralizing Ab STAT IMMEDIATELY AVAILABLE
Primary CNS lymphoma is a common CA in advanced HIV and strongly related to ⬜ virus
For this CA, what is the major determinant for how well these pts will survive?
EBV;
[degree of immunosuppression (CD4 count)]
[T or F]
Live Vaccines (MMR, varicella) should be avoided in patients with CD4<200
TRUE
*“Got HIV? get the TIMP APB Vaccine!”
Name all Vaccines HIV+ adults should receive? (7)
*“Got HIV? get the TIMP APB Vaccine!”
- TDaP
- Influenza
- Meningococcus
- Pneumococcus
- HAV
- HPV
- HBV
note: any Live Vaccines(MMR,Varicella) are c❌d if CD4<200
Tx for Chronic Bacterial Prostatitis (2)
Fluoroquinolone6w vs TMpSMx6w
“CBP=PENIS PAIN! PP: when you Pee! when you Cum! on paper! & just to be!”
Chronic Bacterial Prostatitis
clinical presentation (4)
“CBP=PENIS PAIN! PP: when you Pee! when you Cum! on paper! & just to be!”
- [> 3 mo UTI]…PP when you Pee!
- [> 3 mo pain with ejaculation]…PP when you Cum!
- [UApyuria+bacteriuria & Prostate XMnml|hypertrophy|TTP|edema]PP…on Paper!
- [> 3 mo GU pain]… & PP just to be!
“CBP=PENIS PAIN! PP: when you Pee! when you Cum! on paper! & just to be!
Tx[Fluoroquinolone6w vs tMpSMX6w]
Schistosomiasis is a ⬜ most commonly seen in ⬜.
What are the sx?-4
parasitic fluke worm infxn; [sub-Saharan Africa]
- terminal hematuria
- dysuria
- urinary freq
- peripheral eosinophilia
A patient p/w blood in his urine (at the end of his stream), accompanied with dysuria.
This raises s/f ⬜ which is diagnosed by ⬜ and treated with ⬜
urinarySchistosomiasis ; [identification of eggs on urine sediment microscopy] ; praziquantel
How do you workup gross hematuria?
PSGN-PiG and BrIAN are similar, both presenting as gross hematuria s/p URI
Name 2 major discernible factors
[PSGN-PiG ⼀PostStreptococcal Glomerulonephritis Postinfectious Glomerulonephritis] and [BrIAN⼀Bergers IgA Nephropathy]
Onset & [LabsC3 complement]
P: [O: 1-4WEEKS after infxn] [L: C3DECREASED]
B: [o: 1-4days after infxn] [L: C3normal] ⼀C3 normal due to weak complement fixing by IgA
PSGN-PiG & BrIAN are similar, both presenting gross hematuria s/p URI
Compare their Pathogenesis
[PSGN-PiG ⼀PostStreptococcal Glomerulonephritis Postinfectious Glomerulonephritis] and [BrIAN⼀Bergers IgA Nephropathy]
PSGN-PiG & BrIAN are similar, both presenting gross hematuria s/p URI
Compare their [LabsUA & Serum]
[PSGN-PiG ⼀PostStreptococcal Glomerulonephritis Postinfectious Glomerulonephritis] and [BrIAN⼀Bergers IgA Nephropathy]
Contrast Induced Nephropathy (3)
🩻phenomena in which _R_adiocontrast*(NA_R_CO)* (1-2d after exposure) induces vasoconstriction of the afferent arteriole → ⬇︎GFR → [AKI7 days ]
🩻preexisting renal dysfxn and/or preexisting renal hypOperfusion = CIN risk factors
🩻give high risk CIN pts [aggressive IVFNaCl or NaHCO3] before and after radiocontrast
Jarisch-Herxheimer reaction refers to [sx ⬜7] that develop [⬜ hours] after patient takes treatment for ⬜.
Etiology involves ⬜, and JHR treatment = ⬜
- fever
- HA
- myalgia
- rigor
- diaphoresis
- hypOtension
- [rash progression (if 2º syphilis)]
▶[6-48h];
▶[infection from ANY spirochete (Treponema Syphilis , Borrelia Lyme, Leptospirosis)]
▶[widespread bacterial lysis → massive release of bacterial degradation lipoproteins → transient inflammatory response]
▶[supportive (JHR is self limited to 48h)]
After UA/UCx, your next step in working up Gross Hematuria is ⬜
How can you do this? -2
[evaluate Upper and Lower urinary tract]
Upper: CT urogram > [US(alt for CKD)]
Lower: Cystoscopy > [urine cytology(low risk pts)]
Risk factors for [Urinary Tract Malignancy (renal/bladder/prostate CA)] (5)
- 40+ yo
- male
- smoking
- pelvic radiation
- aniline dyes
Salmonellosis gastroenteritis (2/2 salmonella enteritidis) - is typically treated with ⬜ .
What mitigating factors warrant adding abx(Cipro | Bactrim | Ceftriaxone) ? (2)
SOLELY SUPPORTIVE CARE
_________________
- immunoCompromised
- < 12 yo
80 yom with poor functional status and low quality of life, p/w decompensated CKD, but is NOT candidate for hemodialysis
What do you do for this patient?
[Nondialytic Conservative CKD Management]
- [severe CKD + poor functional status + low QOL] → [Nondialytic Conservative CKD Management (focus on palliative, uremia, mineral-bone disease, electrolyte ∆, bp]
- HD can actually worsen QOL in these pts
T or F
In Patients with poor functional status and low quality of life, HD is likely to improve symptoms and prolong survival
FALSE
Pts with preexisting poor functional status and low QOLS are UNLIKELY to get improved sx and/or improved survival with HD = [Nondialytic Conservative CKD mgmt] instead
clinical presentation for [Disseminated histoPLASmosis] - 4
“histoPLASma spreads to PLAS”
- [Pulmonary*→ Granulomas! *]
- [Lymphatic RES involvement(LymphNodes/Spleen/Liver)]
- [Aplastic Anemia pancytopenia2/2 histoPLASma bone marrow infiltration]
- [Skin (Mucocutaneous papules/nodules)]
Dx =[serum histoPLASma Ag] | [urine histoPLASma Ag] immunoassay
Pt s/p penile circumcision develops postprocedural bleeding
management?
apply compressive elastic dressing (direct pressure) to bleeding surgical site, BUT ONLY FOR SHORT TIME (to avoid necrosis)
and then remove [compressive elastic dressing] after hemostasis … and prior to discharge
What new onset comorbidity should you anticipate following renal transplant?
DM
________________
INC insulin excretion and gluconeogenesis by healthy transplanted kidney
Diagnosis? Tx?
candida Intertrigo
(occurs in inguinal/perineal/genital/intergluteal/inframammary)
________________
Topical Antifungals
⬜ can be confirmed with ⬜
_________________
(⬜3) are major risk factors
candida Intertrigo ; KOH exam
________________
obestiy / DM / immunosuppresion
Acute Tubular Necrosis (a type of ⬜ renal failure) is caused by what 3 things?
intrinsic
________________
ATN comes from SIN
Sepsis
Ischemia
Nephrotoxic meds
Between [Prerenal failure] and [Acute Tubular Necrosis -Intrinsic renal failure]
which responds to aggressive IVF?
[Prerenal failure]
Patient s/p severe hypOtension subsequently develops oliguria
Dx?
________________
Management? -4
Acute Tubular Necrosis
- look for muddy brown cast & FENa>2%*
- ________________*
1. Maintain Euvolemia
2. Maintain Electrolytes
3. Maintain Nephrotoxin avoidance (ACE inhibitors/ARBS/NSAIDs)
4. Hemodialysis if AEIOU (ph<7.1/hyperK/intoxication/overload-Fluid/uremia)
Pts with Giardiasis should refrain from attending ⬜ to minimize disease transmission
________________
Tx for Giardiasis? -4
public crowding
[Tinidazole or NiTazoxanide]
➜ [metronidazole (2nd line/kids)]
[paromomycin (1st trimester pregnancy)]
Giardiasis is transmitted via ⬜-2
What are the Risk factors for Giardiasis -3
Fecal-Oral or ingestion
________________
[Contaminated food/water]
[Fecal incontinence with crowding (day care/nursing home/Norris’ apt)]
Immunodeficiency
⬇︎ with hand sanitizer
diagnosis? | tx?-2
[Tinea capitis ring worm]
________________
[PO griseofulvin] or [PO terbinafine]
cp = scaly pruritic erythematous patches of hair loss
Erysipelas, most commonly caused by ⬜, presents as (⬜2) .
The 1st line Tx is ⬜
GASP;
fever + [acute rapid spreading erythema with raised, well demarcated borders +/- external ear involvement]
________________
PCN
Which 2 organisms cause
skin ABSCESS?
MsSA
MRSA
Which two renal pathologies is analgesic nephrophathy associated with?
[AiN (Acute Allergic interstitial Nephritis)] which → [chronic renal papilla necrosis]
Causes of Papillary Necrosis - 9
POSTCARDS
- Pyelonephritis
- Obstruction of urogenital tract
- Sickle Cell
- Tuberculosis
- Chronic Liver disease
- AAAA (Analgesic NSAIDs/ASA/APAP/Alcohol)
- Renal transplant rejection/Renal vein thrombosis
- DM
- Systemic Vasculitis
________________
tx = correct underlying etx
POSTCARDS➜ ischemia_(i.e. BL AiN) ➜ [chronic renal papilla necrosis] ➜ [papilla sloughing] ➜ {[gross hematuria]/ [prOteinuria] / [pyuria with WBC cast] / [neg urine cx] + [renal colic]}
Papillary Necrosis - 5
MOD
POSTCARDS➜ impaired renal perfusion → ischemia (i.e. BL AiN) ➜ [chronic renal papilla necrosis] ➜ [papilla sloughing]
➜ gross hematuria/ proteinuria / [pyuria with WBC cast] / [neg urine cx] + renal colic
_________________
tx = correct underlying etx
Sydenham chorea is one of the Major features of ⬜
Describe Sydenham chorea clinical presentation -4
________________
tx for Sydenham chorea?
Acute Rheumatic Fever
________________
[DANCING: MIND(emotionally labile) / FACE / HANDS / FEET (rapid jerky movements)]
________________
[PCN until adulthood] (to prevent recurrent rheumatic fever)
Acute Rheumatic Fever requires (2M) or (1M/2m) for dx
List the
5 MAJOR clinical features
________________
4 minor clinical features
late sequelae = Mitral regurgitation/stenosis
⬜ is the most late-onset (months/years after exposure) complication of Lyme Disease
How is Lyme Disease diagnosed? -2
[Lyme Arthritis (synovial fluid WBC 20-50K)];
[serum ELISA + Western blot]
________________
septic arthritis = synovial fluid WBC > 50K
⬜ is the most late-onset (months/years after exposure) complication of Lyme Disease
What is the tx for Lyme disease? (2)
[Lyme Arthritis (synovial fluid WBC 20-50K)]
_________________
[DOXY (or Amoxicillin) PO x 28 days]
________________
septic arthritis = synovial fluid WBC > 50K
Acute Cervicitis Tx? -3
________________
Acute Cervicitis dx? -2
CefTriaxone + Doxy(or Azithromycin if Pregnant)
_________________
- NAAT
- Wet Mount
Describe the FeNa in
PreRenal AKI
_________________
Intrinsic Renal AKI
FeNa
preRenal < 1%
_________________
Intrinsic > 2%
Describe Serology for Hepatitis B -8
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
CSAB = RESOLVED HBV
unvaccinated pts acutely exposed to HBV should STILL get vaccinated in addition to the immunoglobulin
What 2 laboratory values are the best diagnostic test for [acute Hepatitis B]?
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
[SAg and Core_IgM]
Patient p/w isolated elevation of [total anti-HBc (Core_TOTAL)] Ab
How should you manage this? -3
[repeat HBV serologies]
–> [obtain [Core_Igm] and LFT] to determine acuity of [window acute HBV]
_________________
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
Patient p/w isolated elevation of [total anti-HBc (Core Ab)]
What does this indicate? -3
- isolated [⇪ Core_TOTAL] = 2 possibilities:*
1a. [acute HBV window] = [⇪Core_Igm]
1b. [acute HBV window with subclinical hepatitis] = ([⇪Core_Igm] with [⇪ LFT])
_________or_________
2.[chronic HBV postwane]: = [only Core_IgG present]
= Years after acute HBV, once SAb has waned from CSAb = ([no Core_IgM] [SAb wanes → no SAb) = only [Core_IgGwhich will keep [Core_TOTAL] elevated]
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
SIADH can range from mild, SEVERE or Euvolemia
What are the sx of SEVERE SIADH?-3
Tx for SEVERE SIADH?
[SEVERE hypOnatremia → SEIZURES / COMA]
________________
[3% Hypertonic Saline]
SIADH can range from mild, SEVERE or Euvolemia
What are the sx of mild SIADH?-3
Tx for mild SIADH? -2
mild hypOnatremia → nausea / forgetful
________________
[Fluid restriction +/- salt tablets]
SIADH can range from mild, SEVERE or Euvolemia
What are the causes of SIADH -6
- CNS ❌
- Lung ❌
- Meds(Carbamazepine|SSRI|NSAIDs)
- Ectopic ADH(SOLC)
- Pain
- Nausea
❌=disturbance
List PERMANENT causes of Urinary Incontinence in the elderly-7
ADPKD - [Autosomal Dominant Polycystic Kidney Dz]
Describe the Disease - 7
ADPKD
Aneurysm (Berry)
Doomed [HTN-(treat w ACEk2 inhibitor) and MVP]
[PrOteinuria AND Hematuria]
Kidney Failure (Early vs. Late onset) - Hepatomegaly occurs if cystic involvement
Differentiation problem = Etx
Image: Renal Ultrasound which = Dx
Explain how Chronic Kidney Disease is related to the 3 indications for Parathyroidectomy
★ CKD [⬇︎1αHydroxylase] →
[⬇conversion of 25-hydroxyvitD to 1-25DihydroxyVitD] ➜ {[⇪ Phosphate retention] ➜ [bind free Ca+]} + (also ⬇︎ renal Ca+ absorption)] ➜ [⬇︎free Ca+] ➜ [( ⇪ PTH secretion) = compensatory 2º hyperparathyroidism]
_________________
★ EVENTUALLY….
[2º HPTH] may progress to [3° HyperParathyroidism AUTONOMOUS PTH SECRETION]➜ [HIGH PTH AND EVENTUALLY HIGH CA+] ➜ [high bone turnover = (⇪ BONE ALP)] ➜
★ [PTH sx = parathyroidectomy]
- Persistently elevated [Ca+> 10.5] , [(P )because of CKD] and [PTH>800]
- Tissue calcification /[calciphylaxis (vascular calcification)]
- Heavy intractable bone pain
Which 2 organisms cause Cellulitis?
poorly demarcated confluent erythema and/or induration involving deep dermis, SQ fat +/- fever
GASP > MssA
_________________
cellulitis: poorly demarcated confluent erythema and/or induration involving deep dermis, SQ fat +/- fever
CDiff treatment = [⬜ or ⬜] x ⬜ days
Which abx are low risk for causing C.Diff infection (4)
tx = [(fidaXomicin PO) or (Vancomycin PO)]10d
“Microbial Fighters Can Cause Crazy CDiff (and taking macrolides, too)”
_________________
7.aminoglycoside
8.tMP-SMX
9.macrolides
10.tetracycline
Reinfections are from persistent spores of the initial strain
“Microbial Fighters Can Cause Crazy CDiff (and taking macrolides, too)”
1. Monobactams
2. Fluoroquinolones
3. Carbapenems
4. Clindamycin
5. [Cephalosporin3G]
6. [Cephalosporin4G]
_________________
7.aminoglycoside
8.tMP-SMX
9.macrolides
10.tetracycline
CDiff treatment = [⬜ or ⬜] x ⬜ days
Which abx are HIGH risk for causing C.Diff infection (6)
tx = [(PO fidaXomicin) or (PO Vancomycin)]10d
“Microbial Fighters Can Cause Crazy CDiff” (and taking macrolides, too)”
1. Monobactams
2. Fluoroquinolones
3. Carbapenems
4. Clindamycin
5. [Cephalosporin3G]
6. [Cephalosporin4G]
Reinfections are from persistent spores of the initial strain
“Microbial Fighters Can Cause Crazy CDiff (and taking macrolides, too)”
1. Monobactams
2. Fluoroquinolones
3. Carbapenems
4. Clindamycin
5. [Cephalosporin3G]
6. [Cephalosporin4G]
_________________
7.aminoglycoside
8.tMP-SMX
9.macrolides
10.tetracycline
Pt presents with signs of Sarcoidosis but rapidly deteriorates after being given steroids
Dx?
histoPLASmosis
Mississippi and Ohio River basins
Describe [Balanitis] -2
_________________
tx?
[infection / inflammation of glans penis (common in uncircumcised infants)] ➜ THICK WHITE DISCHARGE
+/- [concurrent Candida Diaper Dermatitis]
_________________
topical antifungal
Balanoposthitis = inflammation of glans penis AND foreskin
Clostridioides difficile MOD
Ingested spores (transmitted by fecal-oral route) germinate in COLON = become fully functional bacilli ➜ proliferate unchecked when COLON FLORA IS DISRUPTED ➜ [⇪ release of exoToxin A and B] ➜ mucosal inflammation ➜
[PROFUSE WATERY DIARRHEA ≥ 3 LOOSE STOOLS daily]
Pylephlebitis is described as ⬜, and a rare yet devastating complication of ⬜
[infective suppurative portal vein thrombosis] ; intraabdominal infections
Name the 6 systems associated with causing Erectile dysfunction ?
VINCOSddx
Active TB is transmitted up to ___ months before sx even start
what’s the Mgmt for for ppl exposed to Active TB?- 3
3
* * *
1.1 of 2[tuberculin skin test or interferon gamma assay] screening
if …
* * *
2A.[#1 is NEGATIVE] = 2 of 2[tuberculin skin test or interferon gamma assay] screening 8-10 wks later
_________________
2B. [#1 or #2A is POSITIVE] = CXR + [acid fast sputum testing]–>
if BOTH negative –> [latent TB tx],
othwise → [ACTIVE TB tx]
Tx for Neurosyphilis
[aPG 4MU q4H] x 14d
Why is RPR not reliable when a person first acquires syphilis?
There is a possible [false negative RPR result] early in infection - follow with FTA
How do you know when a pt is fully cured from Syphilis?
Must be [4-fold FTA titer DEC] by 12 month mark
Sx of Rabies - 5
[HAPPY RABIES Sx]
HYDROPHOBIA (fear of water triggering Pharyngeal spasms) = PATHOGNOMONIC FOR RABIES!
Aerophobia
Pharyngeal spasms
[Paralysis (Spastic –> Ascending flaccid)] -> respiratory failure within wks
Yankin’ Agitation
Prognosis for Rabies
VERY POOR
ONCE [HAPPY RABIES Sx] START! = Die within weeks
Remember! Post-Exposure Px IgG and Vaccine CANONLY HELP TO PREVENT ONSET OF SX. Once [HAPPY RABIES Sx] starts….it’s Over
Dengue Fever Sx- 3
- {Break Bone MARF[Myalgia/Arthralgia/Retroorbital Pain/FEVER]*}
- [Thrombocytopenia w POSITIVE TOURNIQUET TEST⊕petechiae with 5 min BP cuff inflation]
- [“white on red”Rash]
Mgmt for Hepatits B- 2
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
- OUTPATIENT FOLLOW UP! (most HepB resolves spontaneously! . Only < 5% → Chronic HBV infxn)
- Admit IF SERIOUS DECOMPENSATION ONLY
acute HBV can develop into [Chronic HBV]
What % acute HBV actually develop into Chronic HBV infection?
< 5%
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
Describe oral involvement for [Coxsackie A⼀Hand Foot Mouth disease]
grayish vesicles on the tonsillar pillars and posterior oropharynx that –> fibrin-coated ulcerations
doesn’t have to have hand or foot involvement
From a lab perspective, how do you differentiate CMV from EBV?
CMV will have a [⊝HAMS (Heterophile Ab MonoSpot)]
Identify
Erysipelas from GASP
_________________
[acute rapid spreading erythema with raised, well demarcated borders +/- external ear involvement]
Pt presents with 2 month productive cough
dx?
Reactivation TB
(cavitary UPPER lung lesion)
This is different from Aspiration PNA since Aspiration PNA occurs in LOWER lobes
“patient presenting with TB rule out has abnormal CXR lesion”
Prior to giving abx, how should you confirm [Active TB Infection] diagnosis? (3)
“before giving ATBI abx …confirm ATBI dx with a good sCAN”
3 SPUTUM SAMPLES
sent for
s**putum mycobacterial:
1. [CX (GOLD STANDARD)** ⼀CONFIRMATORY]
2. [Acid Fast Bacillus Smear(_A_ids ATBI dx confirmation)]
3. [Nucleic Acid Amplification Test ⼀CONFIRMATORY]
What is the Cremasteric Reflex?
________________
Why is it important?
stroking upper inner thigh ➜ testicle elevation
________________
ABSENT CREMASTERIC REFLEX = TESTICULAR TORSION
(6 HOURS UNTIL IRREVERSIBLE DAMAGE)
clinical features of Rocky Mountain Spotted Fever -4
RMSF
▶[Rickettsia Rickettsiioverlaps🔗🇪hrlichiosis] /
▶[Mental AMS❌(a/b HA)]/
▶[Spotted(🆚 macular) RASH@Wrist & Ankles(2/2 thrombocytopenia petechiae) in Summer after Tick Bite]/
▶File❌(fever, [thrombocytopenia w petechiae])
Rocky Mountain Spotted Fever
🇪hrlichiosis = Ehrlichiosis = Rocky Mountain Spotted Fever… without the “SpottedRash” = RMF
recite the order of Initial mngmt for Meningitis-4
FBLA
1st: Fluid Resuscitation
2nd: Blood Cx
3rd: Lumbar puncture BEFORE ABX (unless pt requires Head CT 1st or is critically ill and can’t receive lumbar puncture)
**4th**: Abx Empirically
A Single ring-enhancing Brain Abscess in immunoCOMPETENT pt results from what organisms?-2
________________
How would you diganose this?
[Staph Aureus] vs [Strep Viridans]
________________
CT-guided aspiration for cx
Toxo and Nocardia would occur in immunocomp pts
You find this MRI in an immunocompromised pt
Identify Disease
PML (Progressive Multifocal Leukoencephalopathy) 2/2 [John Cunningham Polyoma Virus]
Hydatid Cyst with eggshell calcification are caused by _______.
________________
What is the definite host for this?
Echinococcus granulosus
________________
DOGS
Pyogenic liver abscess follows after what 2 events?
[Appendicitis (GI infection)]
Surgery
Describe the cutaneous manifestation of blastomycosis
[well circumscribed raised violaceous (wart like) nodules –> microabscess]
Blastomycosis causes Skin, Pulmonary and Bone findings
Diagnosis?
[NeuroCystiCercosis from Taenia Cestode Helminths]
How does transmission of Hydatid cyst to Humans occur?
Echinococcus Granulosus Hydatid Cyst
[EH] reside in sheep(intermediate host)
Dogs eat Sheep ➜ Dog poop now contains [Ee]. → Dog poop contaminates [Human water/food] with [Ee].
Humans consume water/food contaminated with Dog poop⼀[Ee].
[Ee] hatch in human small intestine,
[Ee] penetrate [human small intestinal wall] and travel to Liver where [EH] form
________________
Dx = US / Tx = [Cyst<5cm=Albendazole]
🔎EH = Echinococcus Granulosus Hydatid Cyst
🔎Ee = Echinococcus Granulosus eggs
Where are the most common sites for Kaposi Sarcoma?- 4
- Mouth
- Face
- Genitals
- Legs
papules –> violaceous plaques or nodules
A HealthCare Worker, unvaccinated to Hepatitis B, has just been acutely exposed to Hepatitis B, and now presents with [positive S and E antigen (SEC)] serology
What do you give them? - 2
In the absence of a Source patient, assume Source patient is ⊕ =
[Source patient ⊕] + [unvaccinated HealthCareWorker] =
- Hep B Immunoglobulin
- Hep B VACCINE still
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
A HealthCare Worker, unvaccinated to Hepatitis B, has just been acutely exposed to blood from a [HBV⊝ source patient].
What should you give the Healthcare Worker?
[Source patient ⊝] + [unvaccinated HealthCareWorker]
Hep B VACCINE
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
A HealthCare Worker, [immune to Hepatitis B by vaccination], has just been acutely exposed to blood from a [HBV⊕ source patient]
What should you give the Healthcare Worker?
[Source patient HBV ⊝/⊕] + [any vaccinated HealthCareWorker] =
NOTHING!
[S - SEC - SCEb - corem - CEbSAb - CSAb - coreG - SAb]
Dx? - 2
- [EBV(⊕HAMS, ⊕PANcytopenia)]
- CMV
Which organism should you suspect if a pt with PNA also c/o Diarrhea?
Legionella
What are the risk factors for TB - 4
- Homelessness
- Alcoholism
- Immunosuppression
- Healthcare worker
Disseminated TB affects peritoneum, cervical lymph nodes, eyes, bones and skin
What are the generalized signs of ANY [congenital TORChHH] infection - 3
- Hepatosplenomegaly
- Blueberry muffin spot rash
- Jaundice
Hepatosplenomegaly, [Blueberry muffin spot rash] and Jaundice are sx present in ANY congenital TORChHH infection
Name the 9 [congenital TORChHH] members
Toxoplasmosis
Others(VZV|Parvovirus|Syphilis)
Rubella
CMV
hepatitis
HIV
HSV
LEProsy is a [chronic mycobacterial granulomatous disease]
How does LEProsy present?-3
________________
Dx?
LEProsy
1. [LAD painful]
2. [EM-LIKE ANESTHETIC mascular rash📖]
3. [Poorly functional nerves w ⬇︎s/m]
________________
[Dx = FULL THICKNESS Skin bx of lesion]
[Tx = Rifampin WITH Dapsone] || [hypOfunctional n with ⬇︎sensory/motor]
📖Anesthetic EM-LIKE mascular RashhypOpigmented with raised borders - similar to Erythema Multiforme but more irregular
LEProsy is a [chronic mycobacterial granulomatous disease]
Tx? - 2
- Rifampin WITH
- Dapsone
{[LAD] [EM-like rash] [Poor nerves] ⼀rosy}
Which bacteria is described as Rocky Mountain Spotted Fever without the spots?
________________
What other major lab findings are associated with this bacteria? -3
🇪Ehrlichiosis = Rocky Mountain Spotted Fever… without the “SpottedRash” = RMF
🇪RMF
▶ehRlichiosisoverlaps🔗Rickettsia Rickettsii but has NO RASH /
▶Mental AMS❌(a/b MALAISE)/
▶File❌(Low platelet, Leukopenia, LFTitis)
🔎LFTitis = transaminitis
Dx?
________________
Mode of Transmission?
{[HOOKWORM Ancylostoma Duodenale] [Cutaneous larvae migrans]}
________________
walking barefoot in contaminated sand or soil
Tx = Ivermectin
“ROUND, HOOK, WHIP … intestinal Helminths”
- [ROUNDWORM ascaris Lumbricoides]
- [HOOKWORM ancylostoma Duodenale]
- [WHIPWORM trichuris Trichiura]
Dx?
________________
Tx?
{[HOOKWORM Ancylostoma Duodenale] [Cutaneous larvae migrans]}
________________
Ivermectin
acquired by walking barefoot in contaminated soil|sand
“ROUND, HOOK, WHIP … intestinal Helminths”
- [ROUNDWORM ascaris Lumbricoides]
- [HOOKWORM ancylostoma Duodenale]
- [WHIPWORM trichuris Trichiura]
Sporothrix Schenckii is a ____ fungus found in ____
How does it clinically present?
dimorphic ; decaying plant and soil
papule at inoculation site ulcerates and drains odorless nonpurulent fluid. This then spread proximally along lines of lymphatic drainage
Tx = PO itraconazole
Describe the type of rash you’ll see with secondary syphilis
Diffuse Maculopapular rash starting at trunk and spreading to extremities TO INCLUDE PALMS AND SOLES
Progressive Multifocal Leukoencephalpathy etx
[JC polyoma virus] reactivation in HIV pts –> ASYMMETRIC focal nonenhancing white matter brain lesions WITH NO EDEMA
HIV neurocognitive disorder will have DIFFUSE enhancement
What organism causes Acute Epididymitis? - 3
EColi if >35yo (secondary to bladder outlet obstruction)
________________
[Chlamydia or Gonorrhea if under 35 yo (secondary to STI)]
Ludwig angina is a rapidly progressive cellulitis of the ⬜ and ⬜ space
________________
What is the source of infection?
sublingual and submandibular
________________
infected mandibular MOLAR
What are the major organisms that cause [contact lens keratitis]?-2
_________________
cp? -3
- Pseudomonas
- Serratia
_________________
painful red eye and corneal opacification with corneal ulceration
etx for hordeolum
________________
tx?
[external hordeolum stye]
an external hordeolum = a stye = inflammation of eyelash follicle or tear gland –> tender nodule at lid margin
________________
tx = warm compresses
etx for Miliary TB
_________________
describe the radiograph
Hematogenous spread of TB (possibly from primary infection or reactivation) that –> subacute sx +/- extrapulmonary(CNS, Liver) involvement ;
Millet seed diffuse reticulonodular pattern
cp for Toxic Shock Syndrome-3
________________
What are the causes of Toxic Shock Syndrome?-3
- Diffuse erythematous macular rash
- hypOtension
- fever
__________________
tampons, nasal packing, post surgery
T or F
Lactose intolerance is associated with weight loss
FALSE
histologic findings of Celiac Disease- 3
- intraepithelial lymphocytic infiltrates
- loss of villous architecture -> villous atrophy
- Crypt hyperplasia
bx from distal duodenum
Any RPR Titer greater than ___ is high syphilis titer (positive result)
1:16
anything where they had to dilute it MORE than 16 times is HIGH RPR Syphilis titer
Patients diagnosed with Molluscum contagiosum should be co-tested for ⬜
MC transmission via skin-to-skin contact
HIV (especially if facial MC)
What are the 3 major risk factors for developing [Clostridioides Difficile diarrhea]?
[Abx (“Microbial Fighters Can Cause Crazy CDiff (and taking macrolides, too)” )]
gastric acid suppression
≥65 yo
_________________
CDI ➜ Severe CDI ➜ FULMINANT CDI
⬜ is a gram ⬜ organism most commonly a/w human bite wounds
_________________
Tx for this bacteria? (3)
Eikenella corrodens ; gram negative anAerobe
_________________
- TETANUS PX
- [PO amox/Clav(or IV amp/Sulfa)]
- {TECH woundsleft open to heal by 2º intention*unless [(human|cat) to face]⚠️*}
___________________________x____________________________________
⚠️[(human|cat) face wounds]: [1º healing < 24h old < 2º healing ]
tx for human bite wound? (3)
- TETANUS PX
- [PO amox/Clav(or IV amp/Sulfa)]
- {TECH woundsleft open to heal by 2º intention*unless [(human|cat) to face]⚠️*}
covers polymicrobial + Eikenella Corrodens
⚠️[(human|cat) face wounds]: [1º healing < 24h old < 2º healing ]
wet mount shows: Pear shaped motile organisms
What would you expect vaginal pH to be for this dx?
pH >4.5
dx = Trichomonas vaginalis
_________________
Trichomonas vaginalis in prepubescent child = sex abuse and must be reported
Vibrio vulnificus is a free-living, gram ⬜ bacteria found ⬜. Infection occurs via (⬜2)
_________________
Patients with ⬜ have ⇪ risk for developing what 3 serious sequelae of VV?
negative; marine; [ingestion or wound contamination]
_________________
chronic illness =
- [rapidly progressive {within hrs} cellulitis] -image
- hemorrhagic bullae
- septic shock
* dx = blood/wound cx | tx = IVAbx STAT*
Diphtheria is caused by ⬜
_________________
How does it present? (3)
Corynebacterium diphtheriae
_________________
- [Pharyngitis with grey exudates that coalesce into a {pseudomembrane (bleeds with scraping)}]
- Cervical LAD
- TOXIN-MEDIATED SEQUELAE ⼀ MYOCARDITIS / NEURITIS / NEPHRITIS
cp of TB meningitis (4)
▶[2 weeks low-fever prodrome] ➜
▶[Choroidal tubercles (yellow/white nodules near optic disc)]
▶[basilar meningeal enhancement]
▶{TB CSF: [ADA ⇪ + ( G<45 | P 100-500 | WLymphocyte 100-500⇪)]}
ADA = Adenosine DeAminase
Dx = {⊕CSFAFB smear/culture via [serial LP CSF]}
How do you diagnose TB meningitis ?
{⊕CSFAFB smear/culture via [serial LP CSF]}
[serial LP CSF exams] looking for acid-fast bacilli using smear/culture
What is the treatment for TB meningitis? (2)
[CRiP (A|F)]2 ➜ [Ri]9
_________________
[CTS (prednisone|dexamethasone) / Rifampin / iNH / Pyrazinamide (Aminoglycoside IV or Fluoroquinolone)]2
➜
[Rifampin / iNH]9
HIV PostExposure Prophylaxis can be initiated up to ⬜ hours after exposure , taken for duration of ⬜ and consist of what [4-step protocol]?
[72h (preferably within 3h if occupational)]; 28days
_________________
PEP PTSD
- Primary labs [HIV testexposed (+ HIV testSOURCE)]
- [Triple ARV ([2 NRTI + (1 [II or PI or nNRTI])within 72h]28d
- Secondary labs (HIV testexposed) at 6w
- Delayed labs (HIV testexposed) at 16w
Herpangina
clinical features (3)
- Coxsackie A
- POSTERIOR oropharyngeal vesicles
- [self limited to 1 week (so tx = hydration/analgesics)]
What is Ecthyma gangrenosum? (2)
- Pseudomonas skin lesion [≥1 erythematous macule ➜ blueish/green pustule/bullae ➜ nonpainful gangrenous ulcer]
- immunocompromised pts
Ecthyma gangrenosum
Mgmt (3)
- STAT blood and wound cx ➜
- ([Pip/tazo βL] + [gentamicin aminoglycoside])
_________________
βL=βeta Lactam
Which contacts should receive prophylaxis after Neisseria Meningitidis exposure (4)
- [Livingmate(Roommate/Housemate)]
- Day care workers
- [direct exposure to oropulmonary secretions (i.e. MD that intubates/CPR/Spouse)]
- [seated next to affected person ≥8h]
Name clinical features of this diagnosis (5)
- Scabies*
1. [HIGHLY CONTAGIOUS (via contact) Mite infestation] ➜
2. SEVERE pruritic excoriations with small red crusted papules and linear burrows on the
3. flexor wrist, lateral fingers, finger webs
4. dx by [skin scrapings demonstrating mites/ova/feces under light microscopy]
5. tx = [Permethrin 5% topical cream] (apply everywhere except head) - oral Ivermectin is alternative*
Clostridium Botulinum
MOD
[(spores = babies) | (NEUROTOXIN = ADULT)] ➜
inhibits PREsynaptic ACh release at neuromuscular junctions ➜ [descending flaccid paralysis]
_____________
dx = + serum toxin
[Fulminant Clostridioides Difficile Infection] requires different therapy such as (⬜2) .
_________________
What is the diagnostic criteria for [Fulminant CDI]?
[Vanc PO and Metronidazole IV] –(if refractory)–> [fecal transplant 🆚 surgery]
_________________
Neisseria Meningitidis
What prophyalaxis is given? (3)
Rifampin PO > [cipro PO = Ceftriaxone IM]
_________________
[cipro PO or Ceftriaxone IM] for any Rifampin ctd (ie on OCP)
HIGH risk contact with HIV warrants HIV prophylaxis
What constitutes exposure to HIV as HIGH risk contact? (9)
1. BLOOD
2. (any bodily fluid with visible BLOOD in it)
3. RECTUM
4. SEMEN
5. Vagina
6. Breast Milk
7. Mucous membrane
8. Non-intact skin/Percutaneous exposure
9. eYE
_________________
HIVhRC indicates [HIV PEP PTSD]
low risk contact with HIV does NOT warrant HIV prophylaxis
What constitutes exposure to HIV as low risk contact? (5)
HIV PostExposure Prophylaxis can be initiated up to ⬜ hours after exposure and is taken for duration of ⬜
For [HIV PEPPTSD] name the 3 drugs typically used for the Triple ARV
ARV = AntiRetroViral
[72h (preferably within 3h if occupational)]; 28days
_________________
[(Tenofovir + Emtricitabine) + Raltegravir]
_________________
PEP PTSD
[Triple ARV ([2 NRTI + (1 [II or PI or nNRTI])within 72h]28d
Clostridium Botulinum
Tx
[Equine serum 7valent boTulinum antiToxin]
dx = + serum toxin
recite the [Renin-Angiotensin-Aldosterone] pathway -4
[Angiotensin 1] is converted to [Angiotensin 2] by ⬜
Name all 6 functions of [Angiotensin 2]
[ACE from Lungs]
_________________
“Angiotensin 2 HAVDEN way for more!”
- Hypothalamus: stimulates Thirst at hypOthalamus
- [ADH Vasopressin] secretion from POST Pit → INC principal cell H20 channels
- Vasoconstriction(via smooth m AT1 R)
- alDosterone secretion from adrenal gland
- Efferent arteriole constriction( ⇪ GFR to preserve renal function during low volume states
- [Na+/H+ PCT pump] activity INC → INC PCT Na+ reAbsorption
[AT1R] = Angiotensin 1 Receptor
