Emerg Flashcards
Criteria for consideration of termination of resuscitation
All of the following present:
1) Arrest not witnessed
2) No bystander CPR
3) No ROSC before transport
4) No shock delivered before transport
Epinephrine dose in asystole/PEA
1 mg IV/IO every 3-5 min
Epinephrine dose in anaphylaxis
1:1000 epinephrine
0.01 mg/kg, max 0.5mg
Every 5-15 min as needed
Autoinjector doses for various weights
<10kg –> 0.1 mg dose (Auvi-Q)
10-25 kg –> 0.15 EpiPen Jr
25+ –> 0.3 mg EpiPen
After 3 shocks for VF/pVT, consider what meds?
Amiodarone 300 mg IV/IO followed by 150 mg
Lidocaine 1-1.5 mg/kg IV/IO followed by 0.5-0.75
Ddx mnemonic for symptomatic/unstable bradycardia
Don’t led bradycardia patients DIE
Drugs
Ischemia
Electrolytes
(also many others)
Crystalloid fluid bolus quantity in critically ill patient (w/out fluid overload condition like CHF or advanced renal failure)
30 ml/kg (2-4 L in adults)
Initial management of patient with suspected sepsis (11)
2 large bore IVs
Lactic acid
Initial fluid bolus of 30 mL/kg over first 3 hours
CBC
CMP
2 sets blood cultures
CXR, EKG
Continuous sat monitoring/supplemental O2
Urinalysis w/ culture + pregnancy test in WOCBA
(LP if meningitis suspected)
Empiric ABs (ideally after blood cultures obtained)
(Pressors if continued high lactate or hypotension after fluid bolus)
Example of antibiotic approach to sepsis with source unclear?
Pip/tazo (broad spectrum GN, covers pseudomonas, tazo is B-lactamase inhib)
Vancomycin (GP/MRSA, quite narrow-spec)
Amikacin (aminoglycoside)
Diagnostic criteria for ARDS
1) Acute onset
2) Bilateral infiltrates on CXR consistent w/ pulmonary edema
3) Pulmonary artery wedge pressure <18 mmHg or clinical absence of left atrial hypertension - i.e. resp failure not accounted for by heart failure/fluid overload
4) Hypoxemia with PaO2/FiO2 <300 (ALI) or <200 (ARDS)
What test should be done post-cardiac arrest? If pt can’t follow commands what should be done?
EKG (cardiac ischemia may be cause of Vfib)
Comatose –> targeted temperature management (hypothermia 32-34C for 24-28hrs), EEG
Trauma resuscitation principle that reduces bleeding and improves outcomes (regarding vitals)
Permissive hypotension
SBP goal is 85-90 mmHg (preserves perfusion to brain + vital organs)
- note: permissive hypotension shouldn’t be applied to hypotensive trauma pts w/ mod-severe TBI bc low BP can increase secondary brain injury
Target MAP in septic shock management
Target urine output
Target CVP
MAP 65+
>0.5 mL/kg/hr
CVP 8-12 mmHg (normal range)
MAP formula
=2DBP + SBP / 3
If pt remains in shock after fluid resus, what pressors are given?
Norepinephrine (Levophed) drip
2nd line: vasopressin (improves cellular response to catecholamines)
If STILL doesn’t work –> corticosteroids
Initial issue that should be immediately managed in DKA?
Fluid deficits (can be up to 10L!)
2L saline bolus in adults
10-20 mL/kg saline in children
DKA: rehydration + insulin will lower serum glucose faster than clear ketones. Insulin infusion should be continued until when?
Until anion gap returned to normal
Add dextrose to IV infusion when glucose falls to ~15 to prevent hypoglycemia
What type of insulin do you give during DKA?
Short-acting (Regular)
___ replacement is often necessary before hypokalemia can be reversed
Mg (deficiency increases ROMK K+ secretion)
___, ____ ,and ____ confirm the diagnosis of DKA and are enough reason to start ____. Some providers prefer to wait for a ____ level before starting ____
Hyperglycemia, ketosis, and acidosis
Start fluids
Wait for K+ levels before starting insulin
DKA patients are almost always ___- and have significant ___ and ___ deficits regardless fo specific lab values
Dehydrated
Sodium/potassium
Antidote to beta-blocker overdose
Glucagon (increases HR/contractility bypassing beta-AR site)
True anaphylaxis is a ____ hypersensitivity reaction occurring after a previous sensitizing exposure
vs anaphylactoid?
Type 1
IgE-mediated activation of basophils/mast cells –> PG + leukotriene + histamine release
Anaphylactoid has release of these compounds through non-immune-mediated pathways so doesn’t require prior sensitization
Diagnosis of anaphylaxis
Any 1 of the following 3 criteria:
1) Acute onset w/ reaction of skin or mucosal tissue PLUS resp Sx or hypotension
2) Acute onset of 2+ of the following after exposure to a likely antigen (skin-mucosal tissue, resp, hypotension, GI)
3) Acute hypotension after exposure to known allergen (faintness, AMS)
No response to 3 epipens in anaphylaxis –>
IV epinephrine (2-10 ug/min for adults) *Can cause MI in pts w/ CAD
Give an example of a SAMA and a LAMA
SAMA: ipratropium bromide
LAMA: tiotropium bromide
Role of H1 and H2 antihistamines (and examples) in anaphylaxis
H1 antagonists such as cetirizine or diphenhydramine can be given for cutaneous symptoms (no affect on resp/CV/GI)
H2 (ranitidine) in combo with H1 for better cutaneous treatment
Diphenhydramine for vomiting
Big diff between first gen and 2nd gen H1 antihistamines?
First gen have central effect (sedating)
2nd gen used more as antiallergic
H2 antihistamines are indicated primarily for…
gastric reflux (block H2 receptors in parietal cells of gastric mucosa)
Cetirizine (Reactin), fexofenadine (Allegra) and loratadine (Claritin) are what type of antihistamine
2nd gen H1
Risk factors for severe anaphylaxis (4)
Hx of poorly-controlled asthma or COPD
Advanced age
Pregnancy
B-blocker or ACEi use
STEMI is a ___ infarct, NSTEMI/UA are ___ infarct/ischemia
Transmural
Subendocardial
STEMI is diagnosed when ST elevation is found in __ continuous ECG leads
2+
ACS management mnemonic
MONA greet chest pain at the door (immediate) Morphine Oxygen Nitroglycerine Aspirin 162 mg!!!
BASH later Beta-blockers ACEi/ARB Statins Heparin (e.g. enoxaparin = LMWH)
BOERHAAVE SYNDROME:
Barotrauma induced rupture of the esophagus, usually caused by vomiting.
Initial treatment of Boerhaave syndrome (if perforation is contained)
NPO status NGT placement w/ suction Broad-spectrum IV antibiotics Parenteral nutrition Analgesics + antiemetics urgent surgical consultation!
Treatment of uncomplicated pericarditis
Analgesics
NSAIDS
Colchicine
Define Mallory Weiss tear
Complications? (3)
Tear in mucosal layer @ esophageal-gastric junction
GI hemorrhage, intramural esophageal hematoma, perforation
1/3 of afibers are “lone Afibers” (no clear cause)
The most common causes are what?
PIRATES PE Ischemia (MI) Resp disease (e.g. COPD) Atrial enlargement/myxoma (atrial tumor) hyperThyroid Ethanol Sepsis/Sleep apnea
Also, systemic idsease (obesity/metabolic syndrome, diabetes)
CV diseases: CAD, Htn, valvular diseases, cardiomyopathy
Tenets of treating afib (4)
1) Address overall clinical status/instability
2) Determine/treat cause
3) Control rate and/or rhythm
4) Prevent thromboembolism
In the ED, ___ is generally the first priority in treating AFib
Ventricular rate control
Afib patients with valvular Afib, risk factors for stroke, or duration > ___ get what anticoag?
Duration > 48hrs
Therapeutic OAC 3+ weeks before cardioversion OR TEE to exclude LA thrombus (+enoxaparin)
+ anticoagulation 4 weeks post-cardioversion (long-term based on CHADS-65)
2 best drugs for rate control of Afib in the ED? 2 other options and why they aren’t as ideal?
CCBs & BBs are best (if pt already on something start by trying that)
Digoxin (slow onset, work via vagal mech, not as effective if high SNS tone, won’t control rate during exercise etc; may be combined w/ CCB or BB)
Amiodarone or Dronedarone (antiarrhythmics w/ some BB activity, less effective but could be 2-in-1)
Which CCB/BB has the lowest risk of hypotension and why?
Diltiazem, least negative inotropic effect
Consideration in pt w/ WPW & Afib?
Pharmacological/electrical cardioversion
NOT AV-block agent because can increase accessory pathway conduction –> Vfib
Why is thromboembolism very common post-conversion of AFib?
“Atrial stunning” (delayed onset of atrial contractility after cardioversion, lasts several week)
Or dislodging of old clot
3 exceptions to the 48 hour rule in afib?
Past stroke, mitral valve disease, severe LV dysfunction
Name 2 common drugs used for rhythm control in Afib
Propafenone (Class Ic Na-channel blocker, contraindicated in CAD)
Amiodarone (Class 3 K-channel blocker, preferred if any structural heart disease)
In pts w/ Afib, anticoagulation therapy traditionally consists of ___ with an INR goal of ____. Now what is preferred?
Warfarin
INR 2-3
Now DOACs preferred
Most common precipitant of acute HF exacerbations
Ischemia/infarction or noncompliance with meds/dialysis/diet
Name 1 specific cause of acute left HF and 1 specific cause of acute right HF
Left: sympathetic crisis w/ hypertension (increased afterload)
Right: pulmonary embolism
Name 3 causes of high-output HF
Thyrotoxicosis, anemia, AV fistulas (decreased PVR)
Name 2 causes of peripheral edema other than CHF
DVT
Hypoproteinemia (liver failure, nephrotic syndrome, renal failure)
Things that may be seen on CXR in heart failure in order of increasing L atrial pressure
Upper zone vascular redistribution (“cephalization”)
Kerley B lines (near costophrenic angles; =interstitial edema)
Perihilar “batwing” appearance (alveolar pulmonary edema)
Patient with CHF presenting with hypotension and poor perfusion (i.e. ____) may require what 3 therapies?
Cardiogenic shock
1) Inotropes (dobutamine or milrinone to enhance myocardial contracility)
2) Vasopressors (NE for coronary diastolic perfusion by increasing DBP)
3) Small fluid bolus (increase preload)
Patient with CHF exacerbation involving resp distress and very high blood pressure likely has…
Cardiogenic pulmonary edema secondary to catecholamine surge (hypertensive emergency)
What is the goal & treatment for Cardiogenic pulmonary edema secondary to catecholamine surge (hypertensive emergency)
Redistribution of fluid from pulmonary circulation to rest of body
1) Oxygenation
2) Reduce preload & afterload
3) Diuresis (only after adequate afterload reduction if pt clinically volume overloaded)
2 ways to reduce preload/afterload in cardiogenic pulmonary edema?
BiPAP (preload/afterload)
Nitroglycerine (preload/afterload)
ACEi (afterload)
____ is no longer recommended as standard therapy for CHF
Morphine
Approach to hypertensive encephalopathy
1) NCHCT to rule out mass lesion/stroke
2) IV antihypertensives to lower MAP by 10-15% in first hour, no more than 20-25% by end of first day (not to normal range!) - e.g. nicardipine (DCCB) or labetalol
General approach to hypertensive urgency
Reduce BP over days to weeks
Discharge from ED, f/u outpatient in 24-48 hrs
Examples of evidence of acute end-organ damage in hypertensive emergency
REtinal hemorrhages
Cerebral infarction/hemorrhage, encephalopathy (altered AMS)
MI, aortic dissection, acute LV failure (chest pain, dyspnea)
Acute pulmonary edema (e.g. dyspnea)
Acute renal failure (e.g. anuria)
Microangiopathic hemolytic anemia
Preeclampsia/eclampsia
According to traditional teaching, what drug is contraindicated in cocaine/sympathomimetic intox?
Beta-blockers (unopposed alpha stimulation –>vasospasm)
**newer research indicates may not be true in humans
Gold standard imaging to diagnose/rule out aortic dissection?
CTA
What is Cerebral Perfusion Pressure? (CPP) Significance of this in management of hypertensive emergency in a chronically hypertensive patient?
Proxy for Cerebral Blood Flow used for monitoring (can’t measure CBF directly)
CPP = MAP-ICP
CBF is being maintained at a higher CPP, so if you reduce MAP too fast –> cerebral hypoperfusion
Preferred antihypertensive for preeclampsia/eclampsia
Hydralazine
Acute cerebral infarction in the context of hypertensive crisis - general approach to BP management?
Acutely elevated BP often necessary to perfuse watershed areas, so generally don’t lower acutely
(cautious lowering if >220/120 may be ok)
EXCEPTION is if candidate for thrombolysis, then lower below 180/105
In ACS should beta blockers be administered immediately?
Better to wait until hemodynamically stable bc can exacerbate LV failure
What is the only hypertensive emergency where rapid, aggressive BP reduction is indicated? Why? BP & HR target?
Aortic dissection - need to reduce shear forces of LV ejection (prevent extension of dissection)
SBP 100-110
HR <60
First line medication for aortic dissection hypertensive emergency? 2nd line if BBs contraindicated?
Beta-blockers (simultaneously lower HR & BP)
CCB is 2nd line if can’t use BB
Delayed phase of asthma is more ____ and can be targeted with ____
Inflammatory
Corticosteroids
5 main classes of agents for acute asthma
1) Oxygen
2) Adrenergic agents (preferable inhaled salbutamol; epi or terbutaline if can’t inhale)
3) Anticholinergic (ipratropium bromide = SAMA)
4) Corticosteroids
5) Magnesium sulfate
Induction agent of choice for IPPV (or sedation during PPV if can’t tolerate fully awake)
Ketamine (catecholamine release, bronchodilation)
An asthmatic patient who is intubated should be set to promote the goal of…
Pemrissive hypercapnia (high risk for hyperinflation/auto-PEEP, so use low RR/TV, limit plateau pressures)
Asthmatics who are discharged from the ED should receive…
Salbutamol
MDI spacer device
3-10 day course oral steroids (stop based on Sx resolution & self-monitored peak flow)
Best way to assess asthma severity in the ED is history + physical &…
Peak expiratory flow
What is the role of ECG/CXR/ABG in PE diagnosis
Mostly to rule out other etiologies of Sx!
Utility of V/Q scans in PE diagnosis
Many patients with PE have normal V/Q scan (need to factor in clinical suspicion/other tests)
Most beneficial in pts w/ renal failure who can’t have CT contrast (or contrast allergies)
General gold standard for diagnosing/confirming PE? Caveat?
Computed tomography pulmonary angiography (CTPA)
*can lead to false-positives
First line test for DVT?
Venous duplex ultrasonography (esp good for iliac, femoral, popliteal veins)
In what location should DVT be anticoagulated?
Definitely if popliteal or above
Isolated calf DVTs may be anticoagulated (recommended if Hx or RFs) or repeat U/S in 1 week
____ is the preferred anticoagulant for initial treatment of DVT
Enoxaparin (LMWH), self-administered subQ injection patients can do at home
PE has a notoriously vague/variable presentation. What is the most “classic” triad of Sx?
Dyspnea
Pleuritic chest pain
Tachycardia
What is a lung phenomenon that can occur 24-72 hrs after a PE?
Loss of surfactant –> atelectasis, focal infiltrate
The classic but uncommon EKG change in PE?
S1Q3T3
(deep S wave in lead I, Q wave in III, inverted T wave in III (20%). This “classic” finding is neither sensitive nor specific for PE)
What is the PERC criteria. Age component
Pulmonary Embolism Rule out Criteria
In pts w/ LOW risk of PE (Well’s score), if all 8 are absent, then no further workup needed :)
Age cutoff is 50! So anyone 50+ automatically loses on PERC
When is D-dimer useful? What predictive value is this?
NEGATIVE predicted value
i.e. if normal, excludes PE in patients w/ low pretest probability who don’t meet PERC criteria
Imaging for PE diagnosis in pts hemodynamically unstable (definitive imaging unsafe)
Bedside echo (look for signs of RH strain –> presumptive PE diagnosis so you can start treatment)
Can you prescribe BBs and CCBs at the same time?
NO! Both block AV node –> can lead to high degree blockade and significant BP drop
How might the elderly present with pneumonia?
Minimal Sx; AMS, decline in baseline function Often afebrile (may even by hypothermic), tachypnea may be most sensitive sign
Lobar consolidation is typical of what bacteria?
Streptococcus pneumoniae
Klebsiella
Most common causes of CAP
Streptococcus pneumoniae
Mycoplasma pneumonia
Chlamydia pneumoniae
Resp viruses
HAP and HCAP are most commonly caused by?
Gram-negative bacilli: Pseudomonas aeruginosa, E coli, Klebsiella pneumnoia, Acinetobacter
Healthy patients with presumed CAP and no AB use in the past 3 months should be treated with what AB?
A macrolide (azithromycin)
Antibiotic for patients w/ CAP and comorbid disease, AB use in past 3 months, or high risk of macrolide-resistant Streptococcus pneumoniae
Fluoroquinolone (levofloxacin)
or beta lactam (cefpodoxime = 3rd gen cephalosporin) + macrolide
Pts with concern for HAP/HCAP should receive what AB therapy and why?
Concern for multi-drug resistant pathogens. 3 drug combo therapy
1) Antipseudomonal cephalosporin (cefepime or ceftazidime), antipseudomonal carbapenem, or pip-tazo
2) Antipseudomonal fluoroquinolone (e.g. levofloxacin)
3) Anti-MRSA coverage (linezolid or vancomycin)
Good antibiotic for a presumed anaerobic infection (or multibacteria) in pt w/ pneumonia. What kind of patient would be likely to need a drug with a spectrum covering anaerobes?
Clindamycin
Aspiration pneumonia, e.g. alcoholic pt
Foregut, midgut, hindgut structures
foregut = oropharynx - mid-duodenum + liver, biliary tract, pancreas, spleen Midgut = distal duodenum to mid-transverse colon Hindgut = distal-transverse colon to rectum
Where is pain perceived from the foregut, midgut, and hindgut?
Foregut: epigastrum
Midgut: periumbilical
Hindgut: hypogastrium
6 categories of surgical abdo pain
I O HIPI
1) Infectious
2) Obstructive
3) Hemorrhagic
4) Ischemic
5) Perforating (may overlap with hemorrhagic)
6) Inflammatory
Mnemonic for pertinent headache history questions
SNOOP MEETS PREGNANCY Systemic Sx Neurological Sx (focal, AMS, seizures) Old age Onset (sudden) Pattern changes Mornings worse Exertion/posture/sexual activity Exposures (drugs/toxins) Trauma Secondary risk factors (HIV, cancer...) Pregnancy
What is a population that has a very high rate of serious disease (but also high rate of misdiagnosis) when they present with abdo pain? Name 3 common diagnoses in this population
Elderly folks (up to 1/3 may require surgery!) Biliary tract disease, diverticular disease, bowel obstruction
Mortality of mild and severe acute pancreatitis
5% mild
25% severe
Focus in early management of severe acute pancreatitis?
Recognition & prevention of organ dysfunction (e.g. repleting intravascular volume to prevent renal dysfunction)
**AP causes severe inflammation, capillary leakage, 3rd space loss shock
Utility of CT abdo for acute pancreatitis. Safety consideration re contrast?
Not necessary, can be useful if diagnosis uncertain
Can show degree of necrosis/disease severity
**don’t use contrast until volume depletions corrected
Is upper or lower GI bleeding more likely to deteriorate into rapid/large volume hemorrhage? What is the implication of this for most important test in pt w/ GI bleed of unknown source?
Upper more likely to deteriorate –> upper endoscopy the most important test!
What is an important distinction to make rapidly in patients with upper GI bleeds? Why?
Variceal vs non-variceal
Bc if variceal want to give octreotide (somatostatin analogue, causes splanchnic vasoconstriction)
Name 5 differentials for upper GI bleeding
Peptic ulcer disease Varices (gastric/esophageal) Mallory-Weiss tear Esophagitis Gastritis
Name 7 ddx for lower GI bleeding
1) Upper GI bleeding ;)
2) Hemorrhoids
3) Diverticulosis
4) Angiodysplasia
5) Malignancy
6) Inflammatory bowel disease
7) Infectious conditions
Name 4 common ddx for GI bleeding in children
1) Intussusception
2) Volvulus
3) Meckel diverticulum (congenital outpouching of ileum)
4) Polyps
Where is abdominal pain felt in most patients with GI bleeding?
Trick question! Most patients w/ GI bleeds don’t exhibit abdo pain (though important to do abdo exam for peritoneal signs)
As a general rule, a ____ should be given to patients w/ upper GI bleeds to decrease rebleeding rates
PPI
Transfusion of PRBCs should be considered in what patients w/ GI bleeding
1) Hemodynamically unstable after crystalloid infusion
2) Ongoing blood loss
3) Hb <70 (this restrictive transfusion threshold shown to be superior)
Why is vasopressin no longer favoured for treating variceal bleeding? What should be used instead?
Vasopressin has side effects, end-organ ischemia Somatostatin analogue (octreotide) preferred
Temporary control of massive variceal bleeding can be achieved using
Balloon tamponade
Risks of button battery ingestion? Management?
High risk for mucosal burns/esophageal perf if lodged in esophagus
Confirm location with x-ray; if past esophagus/asymptomatic –> expectant management
In esophagus or symptomatic –> surg
Repeat CXRs until cleared
After clearing an esophageal food impaction, what test should you do?
Barium swallow to confirm clearance and r/o esophageal pathology
Most common location of ingested FB in children?
In adults?
Cricopharyngeal narrowing (upper esophageal sphincter, pharyngoesophageal segment) in children In adults, usually lower esophageal sphincter
In patients with FB ingestion, fever, subcutaneous air, or peritoneal signs suggest…
Perforation –> immediate surg conseult!
In general, once an ingested foreign body passes the ____ , it will continue through GI tract and be expelled without incident
Pylorus
If plain films don’t reveal ingested FB, what are 3 other options?
Esophagogram (barium swallow, if perf not suspected), CT, endoscopy (latter can also remove it at the same time)
Treatment for injested sharp object
If in duodenum or proximal –> endoscopic removal (risk of intestinal perf)
If past duodenum, surgical consult and/or serial radiographs
Treatment for foreign body ingestion of “body packing” (illicit drugs)
Rupture may be fatal, do NOT to endoscopy bc may rupture packet
May use whole bowel irrigation w/ peg to hasten packets through GI tract, otherwise surgery to remove packets
Crampy abdo pain and high-pitched bowel sounds are features of what type of bowel obstruction?
Mechanical (not functional)
What type of bowel obstruction does NOT allow decompression? 2 examples? What type of intervention is usually required?
Closed-loop obstruction (blockage proximal & distal, e.g. volvulus, complete large bowel obstruction + competent ileocecal valve)
Usually require surgery
Small and large bowel obstructions: which is more likely to have distention? Which more likely to have vomiting>
Small bowel –> vomiting
Large bowel –> distention
(though both can have either; large less likely to have vomiting bc of ileocecal valve competence in closed-loop obstruction)
3 most common causes of small bowel obstruction?
Adhesions (70-75%)
Malignancy (8-10%)
Hernia (8-10%)
3 most common causes of large bowel obstruction?
Carcinoma (65%)
Volvulus (15%)
Why might a patient temporarily appear to improve clinically as a mechanical bowel obstruction progresses?
At first there is an increase in peristalsis, then activity diminishes –> dilated/atonic bowel proximal to obstruction (less cramps)
Blood flow also increases then decreases –> mucosal breakdown + ischemia
So baiscally spastic pain first, then ischemic/peritoneal pain
What is the significance of localized vs diffuse tenderness in bowel obstruction?
Diffuse due to distention of bowel wall, visceral pain can be resolved by NG decompression/emesis if open-loop
Localized is a BAD sign, usually means closed-loop, necrosis, perforation –> urgent CT
3 main management strategies for uncomplicated small or large bowel obstruction if identified early?
NPO
IV hydration
NG tube decompression
What defines an “uncomplicated” bowel obstruction. What imaging modality can differentiate?
No compromise to intestinal blood flow
May be partial or complete
CT scan
What imaging modality can differentiate mechanical vs functional large bowel obstructions in most patients?
CT scan (if still unclear, can do contrast enema)
Common clinical sign of colonic perforation in LBO?
Severe volume contraction due to inflammation, failure to improve with aggressive fluid management
May or may not have frank peritonitis
Most likely cause of SBO in pt w/out previous abdominal operations?
Hernia
Most acute diarrhea is ___
Viral
Most common cause of traveller’s diarrhea
Enterotoxigenic E Coli
Which type of bacterial diarrhea should NOT be prescribed antibiotics and why?
Enterohemorrhagic E Coli (shiga toxin) –> hemylotic uremic syndrome
Class of drugs commonly used to treat infectous diarrhea?
Fluoroquinolones:
Ciprofloxacin, levofloxacin, norfloxacin
What is a pathogen that can cause watery profuse diarrhea within 4-12 hours of ingestion
S aureus
Name 5 pathogens that commonly cause noninflammatory diarrhea
Enterotoxigenic E coli Staph aureus Rotavirus Norovirus Vibrio cholerae
Name 5 pathogens that commonly cause inflammatory diarrhea (fever, blood, tenesmus)
Salmonella Shigella Campylobacter Enterohemorrhagic E coli, Enteroinvasive E coli C diff
Kidney stone are most common in which sex?
Men (M:W 3:1)
Positional differences bw patients w/ acute abdomen and nephrolithiasis (comfort)
Acute abdo –> supine, still, knees to chest
Nephrolithiasis –> move around, can’t get comfy
Is pain w/ nephrolithiasis constant or colicky?
Can be either
ureteric usually colicky (stretching ureter); renal pelvis/bladder usually asymptomatic but if pain usually constant
Are neophrolithiasis stones radioopaque?
Usually (90%), most stones are Ca-based
Triad of Sx that indicate a medical emergency in nephrolithiasis
Fever, pyuria, severe CVA angle tenderness
pyelonephritis caused by obstruction –> sepsis
2 best imaging modalities for renal colic (older and newer methods of choice_
Traditionally: IV pyelogram
Newer: Helical CT imaging w/out contrast (more sensitive/specific and assesses surrounding structures, although doesn’t show degree of compromised excretion in the kidney like IVP does)
3 main goals of working up nephrolithiasis
1) Pain control
2) Determine degree of obstruction
3) Detect infection
In nephrolithiasis, definitive therapy is determined how?
Based on the types of stones being formed (strain all urine to recover stones)
Indications for urgent urologic consultation in nephrolithiasis
1) Inadequate oral pain control
2) Persistent nausea & vomiting
3) Associated pyelonephritis
4) Large stone (>7mm)
5) Solitary kidney
6) Complete obstruction
Most small stones (<6mm nephrolithiasis) can be managed via…
Conservative management: analgesics, hydration, ABs if necessary
Most patients can go home w. instructions to increase fluid intake & strain urine
When is surgery indicated for nephrolithiasis?
Stone >8mm
Persistent pain
Failure to pass despite conservative management
Name 2 meds that can help pass a stone
Alpha-blocker (Tamsulosin)
Corticosteroids (reduce edema)
Stones in the lower UT can be removed via ____, upper UT stones treated by _____
Ureteroscope
Extracorporeal Shock Wave Lithotropsy
Does degree of hematuria correspond to degree of obstruction (nephrolithiasis)
No! e.g. a complete obstruction could involve 0 hematuria
Testicular torsion can occur at any age but is most common at what ages?
<1yo
Puberty (hormones)
What is a congenital deformity that increases the probability of testicular torsion?
Bell Clapper Deformity
Horizontal lie of testis in scrotum, epididymis & testicle hang freely and can rotate in scrotum rather than being firmly attached
What are some characteristics of the presentations of epididymitis/orchitis that help differentiate them from testicular torsion?
Gradual onset of scrotal pain
Lower UTI Sx (including fever)
Normal anatomical position of testis (but swollen/tender), intact ipsilateral cremasteric reflex
What scrotal pathology involves INCREASED blood flow on color doppler?
Epididymitis
What reliefs pain in epididymitis
Elevating the testicle (Prehn sign)
Is pain on epididymitis or orchitis more sudden
Orchitis more sudden, epididymitis more gradual
Tender nodule/”blue dot sign” on scrotum are characteristic of
Appendageal torsion
Salvage time after onset of pain for testicular torsion
4-6 hours
“Classic” presentation of testicular torsion
Sudden onset severe pain in lower abdomen, inguinal area, or scrotum
Often preceded by physical activity/trauma (though can occur during sleep)
Nausea/vomiting
Horizontal lie of testicle and loss of cremasteric reflex
If uncertain whether there is testicular torsion, what study?
Ultrasound with color Doppler
Treatment for testicular torsion
1) Emergent manual detorsion (try medial to lateral “opening a book” first)
2) Surgical intervention - emergent if manual failed, elective if it worked temporarily
Does pyuria/bacteruria rule out other testicular pathologies?
No! e.g. 50% of patients w/ epididymitis have it, could also still be a torsion
Name 2 med classes that increases risk of hyperkalemia
ACE inhibitor (potassium retention) Potassium-sparing diuretics: aldosterone antagonists (e.g. spironolactones), ENaC blockers (e.g. amiloride)
Meds for hyperkalemia
a) Cardioprotection: Ca
b) Shift K+ into cells: insulin, beta-adrenergics, NaHCO3
c) Remove K+ from body: loop diuretics, sodium polystyrene sulfonate (SPSS)
Normal serum K+
3.5-5
What is a condition that predisposes someone to hyperkalemia?
CKD
Name 6 clinical features of hyperkalemia
Fatigue Weakness Paresthesias Paralysis Palpitations Anorexia/nausea/vomiting
Serum level for severe hyperkalemia –> requires immediate aggressive threatment
7.0+
What can happen if blood sample is hemolysed prior to K+ measurement?
Pseudohyperkalemia (false positive)
*most labs will report this when detected
EKG change in hyperkalemia
"Peaked" T wave (too pointy to sit on!) Wide QRS Long PR/QT ST changes (can mimic MI) Wide/absent P waves Blocks/arrhythmias **HONESTLY ALMOST ANYTHING