PAEA Book Flashcards
NY heart associated functional classification of heart disease
I-no limitation no fatigue dyspnea or angina pain
II- slight limitation of physical activity results in symptoms
III- marked limitation of physical activity; comfortable at rest but less ordinary activity causes symptoms
IV- Unable to engage in any physical activity
Mechanism of hypovolemic shock and 3 examples
Decreased iV volume
Hemorrhage
Loss of plasma
Loss of fluids and electrolytes
Cardiogenic shock and causes
Defective cardia output, cycle of output
Can be the cause of MI Dushythmias HF Defects in the septum Myocarditis Hypertension Cardiac contusion Rupture of ventricular septum Cardiomyopahties
What is and examples of obstructive shock
Blockage of blood flow into or out of the heart
Tensión pneumothorax
Pericardial tamponase
Obstructive valvular disease
Pulmonary problems
Massive PE
Examples of distributive shock
Increase/excessive vasodilation
Examples include Septic shock SIRS Neurogenic shock Anaphylaxis
Third space sequestration would be an example of
Hypovolemic shock
Also see this with loss of plasma or shock caused by hemorrhage
Loss of fluid and electrolyte Balcance
Anything that depletes intravascular volume
What is neurogenic shock
This is a type of distributive shock that is also seen with SEPSIS and anaphylaxis
Spinal cord injuries and adverse effects or spinal anesthesia
This occurs from interruption of the sympathetic vaso motor input after a high cervical spinal cord injury
Can have arteriolar dilation
Can have venodilation causes pooling in the venous system and decreases venous return and cardiac output
How would neurogenic shock differ from other types of shock in terms of symptoms
Extremities are often warm in contrast to the usual sympathetic vasoconstriction induced coolness in hypovolemic or cardiogenic shock
Treatment for neurogenic showcase
Similar to relative hypovolemic and the loss of vasomotor tone
Excessive volumes of fluid may be required to restore normal hemodynamics if given alone
Once rule out hemorrhage can use nerepi or a pure alpha adrenergic agent (phenyephrine) may be necessary to augment vascular resistance and maintain an adequate MAP
Hypoadrenal shock
The normal host response to illness, operation, or trauma requires that the adrenal glands hypersecrete cortisol in excess of that normally required
This happens in the settings in which unrecognized adrenal insufficiency complicates the host response to the stress induced by acute illness or major surgery
This can be seen with administration of chronic steroids
Diagnoses of adrenal insufficiency is established with
ACTH stimulations test
What is the treatment of hypoadrenal shock
Dexamethasone sodium phosphate 4mg IV
This agent is preferred if empiric therapy is required because, unlike hydrocortisone, it does not interfere with the ACTH stimulation test
Septic shock is post commonly asssociated with
Gram-negative and gram-positive sepsis in persons at extrémese of age and persons IC
Do studies for a pt is suspected shock
CBC Type cross Electrolytes Glucose Urinalysis Serum creatinine
These help in determining the cause
ECG, CXR, cardiac biomarkers, BNP
LACTATE
What level of lactic acidosis indicates hyperlactatemia
Metabolic acidosis
Anaerobic metabolism
2-4
What level of lactic acidosis comes with a 75% mortality
5
Inotropes for shock
Dobutamine
Dopamine
Epinephrine
What are the preSSRIs commonly used in shock
Norepinephrine
Vasopressin
Dopamine
Phenylephrine
Definition of orthostatic HTN
Greater than a 20 mm hg drop in systolic BP or a drop of greater than 10 mm Hg in diastolic between supine and sitting
If no change in pulse occurs with orthostatic HTN consider
Medication cause
Parkinson
Shy-drager syndrome
Peripheral neuropathies (diabetic autonomic neuropathy)
How is hypertensive urgency defined
Systolic BP greater than 220 or systolic greater than 125
How is a hypertensive urgenytreated
Must be treated within hours
First line is nicardipine pls esmolol
Nitroglycerin plus beta blocker (if myocardial ischemia is present)
Alternative HTn treatment Enalapril Diazoxide Trimethaphan Loop diuretics
What is the treatment for hypertension in pregnancy
Nicardipine or labetelol
What is HTN emergency
Strikingly elevated above 220 or above 130 with sign
Encephalopathy Nephropathy Intracranial hemorrhage Aortic dissection Pulmonary edema Unstable angina MI Preeclampsia Eclampsia
When is the window of treatment for hTn emergency
BP must be treated within 1 hour to prevent progression of end organ damage or death
Malignant hypertension
Must also be reduced within 1 hour
Strikingly elevated
Usually seen with papilledema
Either nephropathy
Encephalopathy
Complications of untreated HTN
Cardiovascular Cerebrovascular Dementia Renal disease Aortic dissection Atherosclerotic complications
Prehypertension is defined as
120-139
80-90
What a re the loop medications
How do they work for HTN and what do you need to be careful of
These include
Thiazides
And hydrochlorothizide
These reduce plasma volume and peripheral resistance
Need to monitor potassium and other electrolytes
What are the beta adrenergic anatagonist
What a re they and how do they work
AKA beta blockers
These decrease heart rate
Reduce cardiac output
Reduce mortality after MI and heart failure
What pts would you use a beta blocker with and what medication would
Most effective in younger white patients use with caution in diabetes or pulmonary disease
How doe ACE inhibitors work?
Inhibit bradykinin
Degradation
Stimulates synthesis of vasodilating prostaglandins
Reduce mortality after MI in heart failure
Ace inhibitors are the drug of choice in
CKD
DM
CCB is the drug of choice in
Elderly and black patients
When would you use a alpha adrenergic antagonist
Alfuzosin
Or a alpha adrenergic anatagonist
For lowering peripheral vascular resistance
chronic bronchitis
blue bloater
cyanosis
hypoxemia
hypercapnia from the constant presence of peripheral edema
from cor pulmonale (peripheral edema)
chronic cough with large amounts of sputum
ephysema
cachectic appearance without
cyanosis
pursed lip breathing
pink puffer
use of accessory muscles for respiration
shortness of breath is manifested by the pursed lip breathing and the use of accessory muscles of respiration
how do you diagnose COPD
PFT
will see a decrease in FEV1/FVC
no reversibility
can also check a ABG if FEV1<50%
ALL pts should be screened for alpha anti triptin 1 deficiencys
tx copd
SABA PRN
add LAMA
tiotroprium
+LABA (olol)
whata re some of the systmic manifestations of COPD
hyerpcoagulability (stroke , PE, DVT, atrophy)
weight loss osteoperosis skin wrinkling anemia fluid retention
infarction
arrhytmia
congestive heart failure
ddx of COPD
HF asthma tb Bronchiectasis anemia cystic fibrosis neoplasm PE Obliterative bronchiolitis diffuse panbrochiolitis sleep apnea hypothyroidism nueromuscular dz
TREATMENT
corticosteroids
o SpO2 88-88
prevention
Inhaled steroids are reserved for patients copd
with either ≥2 exacerbations annually or FEV 1 <50% of predicted. The role of inhaled corticosteroids (ICS) in COPD is controversial.
what are the absolute CI to thrombolytic therapy
suspected AD
active bleeding
any prior cerebral hemorrhage
intracranial neoplasm
cerebral aneurysm or
arterovenus malformation
ischemic cerebrovascular
accident within 3 mo
relative CI to thombolytic therapy in acute MI
bleeding diatheses coagulopathy
major surgery within 3 wk
puncutre of noncompressible vessel or other bleeding within 2 wk
hemorrhage within 6 mo
proliferative retinopathy
active PUD
history chronic severe poorly controlled HTN (>180)
cardiopulmonary resuscitation
pericarditis s/p STEMI tx
ASA
NOT steroids
most common presentation of myocarditis
flu prodrome
dyspnea -72
chest pain -32
arrhytmias -18
chest pain is pleuritic or positional whenever the pericardium is involved
may have recent flu like syndrome
severe, diffuse and acute with sudden CHF symptoms–?> shock and death
etiologies of myocarditis
MCC IN DEVELOPED COUNTRIED VIRAL COXSAXIE B , (adeno, paro, hepatitis c, Coxs, cytomegalovirus, enterovirus)
bacterial (staph aureus, clostridium perfringens, diptheria, mycoplasma)
mycotic (candidia, aspergillus, blastomyces, histo)
parasitic (trypansoma cruzi MCC world wide)
rickettsia rickettsi
disease processes that can lead to myocarditis
rheumatic fever SLE granulomatosis with polyangitis GCA drugs toxins systemic and collagen vascular disease radiation postpartum
drugs that cause myocarditis
cociane emetine doxorubicin sulfonamides isoniazi methyldopa
DDX OF MYOCARDITIS
CLOZAPINE ischemic caridomyopathy acute coronary syndromes valvulopathies infiltrative disease of the myocardium sarcoidosis amyloidosis hemochromatosis chagas
what is the ddx for myocarditis
ischemic cardiomyopathy and other cardiomyopathies
valvulopathies ACS infiltrative disease sarcardoicosis amyloidosis chagas hemacrhomatosis
dx workup for myocarditis
CXR
ECG
MRI
endomyocardial biopsy GOLD STANDARD?
(not very sensitive 10-35%)
mostly looking at cardiac troponin with 89% sensitivity
Increased CK MB
BNP if HF sxs
can do cardiac MRI
tx for nonpharmacological therapy
supportive care
restrict physcial exercise
BB for peds
IVIG
maybe inotropic drugs if severe enough
bed rest
avoid heavy use of alcohol
NSAIDs should be avoided in patients with HF generally given the risk of HF exacerbation and possible risk of icnreased mortality
antiarrhythmics therapy
why don’t you use NSAIDs for patients with heart failure
pt withs HF are dependent
upon vasodilating prostaglandins to maintain renal perfusion and salt and water balance decrease prostaglandin synthesis and, thus, may precipitate fluid retention in patients with heart failure.
in pts with CHF from myocarditis what is the treatment
ACE inhibitor
BB
possible aldosterone receptor antagonist will decrease their mortality in the long term
what are carcinoid tumors and how do they present
rare neuroendocrine tumors of the digestive tract, lungs, and less commonly of the kidneys and ovaries.
skin flushing, wheezing and diarrhea
24-hour excretion of 5-hydroxyindoleacetic acid (5-HIAA) in the patient’s urine
What medications are used for symptomatic control of carcinoid tumors?
Somatostatin analogues such as octreotide, pasireotide and lanreotide.
———-is the most appropriate selection to use as daily prophylaxis against the anginal pain caused by Prinzmetal (variant) angina.
Amlodipine
treatment for afibb with RVR
intravenous calcium channel blockers (diltiazem, verapamil) or beta-adrenergic blockers (metoprolol) are first-line rate-controlling agents for stable atrial fibrillation.
What agents should be avoided in patients with atrial fibrillation and Wolf-Parkinson-White (WPW) syndrome?
AV-nodal blocking agents such as adenosine, calcium channel blockers, beta-adrenergic blockers, and digoxin. This can lead to cardiovascular collapse due to preferential accessory pathway conduction.
Theophylline is recommended for…. these two dz processes
Theophylline is recommended for pulmonary hypertension and asthma
Name two steroid-sparing alternative medications used for pulmonary sarcoidosis.
Azathioprine and methotrexate.
what are the lab, CXR, and biopsy finding in sarcoidosis
Patient will be an African-American woman
Labs will show hypercalcemia and elevated serum ACE
CXR will show bilateral hilar adenopathy
Biopsy will show noncaseating granulomas
Treatment is steroids
cor pulmonale is the result of
cor pulmonale is the result of pulmonary hypertension associated with diseases of the lung, upper airway, pulmonary vasculature or chest wall. The disease presents as altered structure and function of the right ventricle.
what is the standard lab follow up for a patient on amiodarone
Amiodarone is a class III anti-dysrhythmic drug used to treat many common dysrhythmias. An annual chest radiograph is recommended when patients are on chronic amiodarone therapy.
Several types of pulmonary toxicity may result from chronic amiodarone therapy; however, the most common is a chronic interstitial pneumonitis.
what is the name and the presentation for the acute form of sarcoidosisi
Lofgren syndorme
hilar lymphadenopathy
erythema nodosum
arthritis
RF for aortic dissection>
HTN Advanced age GCA connective tissue disease family hx cocaine abuse iatrogenic pregnancy
MCC of PNA in ED
acute bronchitis
she has been using her albuterol inhaler every 15 minutes for the last four hours without relief. What laboratory abnormality is likely to be found in this patient?
Hypokalemia
put patient therapy for DVT
Enoxaparin
NOT unfractionated heparin ast his requries being hospitalized
A 74-year-old woman presents with complaints of fever, productive cough with bloody sputum, shortness of breath, and headache. These symptoms developed and worsened drastically over the past 3 days. She recently recovered from an influenza infection 1 week ago. Her medical history otherwise includes only well-controlled hypertension. Vital signs on presentation are as follows: T 39°C, HR 106, BP 110/75, RR 30, oxygen sat 95% RA. A chest radiograph is obtained and a subsequent CT scan of the chest demonstrates multiple cavitary lung lesions. Which of the following organisms is most likely responsible for this patient’s presentation?
staph aureus
necrotizing pneumonia
The most common organism in necrotizing pneumonia, particularly after a viral upper respiratory infection, is S. aureus. Necrotizing pneumonia is known to be caused by a specific S. aureus strain that produces Panton-Valentine Leukocidin (PVL). Often, this infection and the ensuing pneumonia that develops, is preceded by an influenza infection. T
what are the HTN medications that should be given in a AA
thiazides and CCB
the treatment of choice in hemodynamically stable wide-complex tachydysrhythmias in WPW syndrome. E
procainamide is
what does legionella pneumonia look like
associated with water sources pleuritic chest apin bradycardia neurological symptoms hyponatremia relative bradycardia
74-year-old woman with a history of heart failure presents to the ED with shortness of breath. Her vital signs are notable for heart rate 105 beats/minute, blood pressure 180/90 mm Hg, and oxygen saturation of 87 percent on room air. Chest X-ray shows pulmonary edema. You are considering starting nitrates. Which of the following underlying conditions puts the patient at risk of developing nitrate-induced hypotension?
as
The term sick sinus syndrome was coined to describe
The term sick sinus syndrome was coined to describe patients with SA node dysfunction that causes marked sinus bradycardia or sinus arrest.
may manifest in syncope and the treatment is a pacemaker IF SYMPTOMATIC
Permanent pacemaker with AICD
DX of pericarditis involves at least two of the following
typical pleuritic chest pain
pericardial friction rub
suggestive ECG
new or worsening pericardial effusion (Beck’s triad)
what is the treatment for pericarditis
high dose ASA
no NSAIDs if recent bleed MI
CHF
renal failure or
Upper GIB
colchicine secon line
dressler’s colchicineor asaparin
kussmaul’s sign
increase in JVP with inspiration
difference between ECG with acute pericarditis vs pericardial effusion vs constrictive pericarditis
diffuse ST= acute
effusion= low voltage QRS complexes
no classic ECG for contrictive but will see calcification on echo
difference in treatment for pericaridal effusion vs constrictive pericarditis
for pericardial effusion you do pericardiocentesis
for constrictive pericarditis you do a pericardiectomy
RF for PAD
smoking
DM
HTN
hypercholestrolemia
MC presentation of PAD
intermitten claudication (aching pain, cramping, weakness, numbeness, heaviness of the leg induced by exercise and relieved with rest)
critical limb ischemia (>2 weeks) rest pain, or tissue loss with nonhealing ulceration, necorsis or gangrene
acute limb ischemia i
what is acute limb ischemia
<2 weeks onset of symptoms due to poor perfusion of the extremities and further categorized by
viable
threatened
irreversible (sever sensory loss and muscle weakness)
physical findings in PAD
diminished pulse
cool skin temperature of lower extremities
bruits heard over the distal aorta
iliac or femoral arteries
changes in skin color
trophic changes like loss of hair or brittle nails
what is the etiology of PID
atherosclerotic narrowing of the arterial lumen that results in impaired blood flow to the lower extremities
symptoms manifest with exercise as metabolic demand increases
critical limb ischemia may develop gradually fro, progressive atherosclerosis or in a subacute fashion from multisegmental atherothrombosis or atheroembolization
ALI <2 week symptoms and poor profussion
ddx of PAD
vasculitis MSK d/o spina stenosis or nerve root compression peripherla neuropathy raynaud's disease reflex sympathetic dystrophy compartment syndrome DVT popliteal entrapment syndrome direct vascular injury
acute bronchitis is MCC by
adenovirus
PE of chronic bronchitis
rales crackles rhonchi wheezing might change with location of the cough
signs of cor pulmonale (peripheral edema and cyanosis)
CXR of chronic bronchitis
increased vascular markings and enlarged right heart
what might you see on a ecg with chronic bronchitis
cor pulomanle will show right ventricular hypertrophy and right atrial enlargement
potentially MAT
anticholinergic use din COPD pts
what is the name and what are the side effects
tiotropium aka spirivia is a LAMA
it blocks acH mediated bronchoconstriction–> bronchodilation
s/e include dry mouth, blurred vision, urinary retention, difficulty swallowing
tiotroprium is CI in pts with
BPH and glaucoma (because they increase urinary retention and pupillary dilation)
staging of PAD
I: asymptomatic II a: mild claudication II b: moderate severe claudication III: ischemic rest pain IV: ulceration or gangrene
first line for establishing a dx of PAD
ABI
calculated by dividing the highest dorsalis pedis or posterior tibial pressure by the highest brachial pressure obtained form eitherthe right or left arm
abnormal is <0.90
normal 1-1.40 at rest
non-compressible/calcified: >1.40
routine screening NOT recommended
PVD vs PAD
pvd is worse with leg dependnecy standing and prolonged sitting
PAD is worse with walking elevation of the leg and cold
better with leg dependency and rest
which type of PVascD has redness with dependency
dependent ubor is seen with PAD
leg ulcers with PVD are seen
medially
uneven margins
leg ulcers wtih PAD
lateral
clean margins
what is statis dermatitis
eczematous rash, thickening of skin and brownish pigmentation
pulses and temp usually normal
seen with PVD
when does rhuematic fever typically occur
usually 2-3 weeks but as late as 5 weeks
most common infection sxs seen in rheumatic fever
carditis 50-70%
arthritis 35-66%
chorea 10-30 %
subcutaneous nodules
major criteria Rheuamtic fever
two major
Joint Oh my heart Nodules Erythema marginatum Sydenham's chorea
minor criteria rheumatic fever
Cafe-CRP increased
A-arthralgia
F- fever
E- elevated ESR
P-prolonged PR
A- anamnesias of rehmatitis
L-leukocytosis
Tx for rheumatic fever
ASA
PNC
corticosteroids
Tx SSS
episodes of dizziness weakness and flushing of the face
pacemaker with AICD
TX Vtach
stbale and unstable
unstable–> synchronized cardiovert
stable–> amiodarone -lidocaine
constrictive pericarditis sxs and tx
right sided heart failure pericaridal knowck
tx
pericardectomy
diuretics
sxs of primary aldsoteronism
HTN
hypokalemia
hypernatremia
metbaolic alkalsosis
ABI for healing ulcers in DM and NOn DM
VENOUS STasis ulcer
.85 DM
.6-.8 NON dm
gold standard of acute arterial occlusion
arteriography
shows length location
degress of occlusion
doppler often used in er
holosystolic murmur heard best at apex radiation to the axilla
mitral valve prolapse MC reason of this (ischemia)
pathophysiology of WPW
accessory pathway that connects atria and ventricles–?electrical signals bypass AV node
short PR interval and wide QRS from DELTA WAVES
in what time span do you need PCI in MI pt
90 minutes or TPA
order of treatment in NSTEMI
1) anti-thrombotic (aspirin, heparin, ADP-inhibitors, GP IIb/IIIa inhibitors, X in)
2) adjunctive (b-blockers, nitrates)
what is the dx test for prinxemetal anginea
coronary angiogram w injection of provocative agents (ergonovine)
ST elevation only tracked while experiencing attack–>why you provac it
what is the PE with mitral stenosis
MCC
sxs
heart sound
MCC is rheumatic heart disease
Right sided heart failure, pulm htn, A-Fib, mitral facies (flushed face)
Diastolic rumble @ apex–>LLD, opening snap
dilated cardiomyopathy clinical presentataion
(ischemic*, genetic, alcohol, postpartum, chemo tox, myocarditis, endocrinopathies, viral)
systolic HF sxs
s3
fatigue
signs of left and right sided CHF lateral displaced mri
what is the tx for dilated cardiomyopathy
Tx: abstinence from alcohol, ACE-I, diuretics, digoxin, B-blockers, salt restriction
stasis dermatitis improves with
elevation and walking
inferior MI leads
- II, III, aVF, RCA
posterior MI leads
ST depression V1, V2
MCC of restrictive cardiomyopathy
amylodosis
dx test with restrictive cardiomyopathy
ECG–>nonspecific with ST seg and T wave abnormalities
Echo–> diated atria and myocardial hypertrophy
amylodosis
CXR–>coronary vascular congestion (normal heart size)
restrictive cardiomyopathy tx
Diuretics–> may be useful if pulm vascular congestion or edema
Patients with ischemic colitis present with
Patients with ischemic colitis present with sudden onset of mild to severe cramping, often on the left side of the abdomen, along with rectal bleeding or bloody diarrhea within 24 hours of symptom onset.
An abdominal CT may demonstrate findings of thickening of bowel wall or free peritoneal fluid
bronchitis symptoms but with fever
think PNA
MCC of bronchitis
viral
cough can be productive or not
do fluids antypyretics rest antitussices bronchodilators Anbx are beneficial in elderly or COPD or IC >7-10
Tx for acute exacerbations of chronic bronchitis
azithromyocin
hypercalcemia and cavitary lesions
squamous cell
Gynecomastia MC with what type of lung cancer
Gynecomastia MC with adenocarcinoma.
Lambert-Eaton Syndrome
associated with small cell. Antibodies against calcium-gated channels @ the neuromuscular junction => weakness similar to myasthenia gravis but in Lambert-Eaton, the weakness IMPROVES with continued use.
pulmonary nodule
Age <30, lesions stable more than 2y
Low prob of malignancy (<5%)–> monitor with CT 3 months
intermediate probability of CA with solid lung nodule
Intermediate prob of malignancy (5-60%)–>
biopsy
(transthoracic needle for peripheral lesions or bronchoscopy for central lesions)
PET+–> high CA
VATS
high probability of malignancy
go straight to staging and resection
no bx
gram stain of strep pneumoniae
Strep pneumoniae, gram + cocci in pairs
cam PNA sxs
Sudden onset of Fever, productive cough, purulent, tachycardia/pnea
Bronchial breath sounds, dullness to percussion, increase tactile fremitus, increase egophony
tx of out pt CAM
Tx: outpatient
Primary Options
azithromycin : 500 mg orally once daily on day one, followed by 250 mg once daily for 4 days
clarithromycin : 500 mg orally twice daily
erythromycin base : 500 mg orally four times daily
Secondary Options
doxycycline : 100 mg orally twice daily
(doxycycline or macrolide )
in patient tx of CAM
B-lactam + macrolide or broad spectrum FQ
azithromycin : 500 mg intravenously once daily
– AND –
ampicillin : 1000 mg intravenously every 6 hours or
cefotaxime : 1 g intravenously every 8 hours or
ceftriaxone : 1 g intravenously once daily
OR
levofloxacin : 750 mg orally/intravenously once daily
moxifloxacin : 400 mg orally/intravenously once daily
ICU non pseudomonal
B-lactam + macrolide or B-lactam + broad spectrum FQ
ampicillin/sulbactam : 1.5 to 3 g intravenously every 6 hours more
or
cefotaxime : 1 g intravenously every 8 hours or
ceftriaxone : 1 g intravenously once daily
– AND –
levofloxacin : 750 mg intravenously once daily or
moxifloxacin : 400 mg intravenously once daily or
azithromycin : 500 mg intravenously once daily
is pseudomonal PNA suspected
antipneumococcal, antipseudomonal beta-lactam
(e.g., piperacillin/tazobactam, cefepime, meropenem)
PLUS
ciprofloxacin or levofloxacin.
PNA related to Related to AC and cooling vacs, contaminated water
legionella
CAM
- Add Levofloxacin or Azithromycin if Legionella is suspected.
what symptoms would you expect to see with legionella
GI sxs: anorexia, N/V/D, increased LFTs, hyponatremia
Chronic fibrotic disease 2ry to inhalation of mineral dust (ingested by alveolar macrophages)
Pneumoconiosis
Restrictive lung disease, decreased lung compliance
progressive massive fibrosis; CXR shows small upper lobe nodules and hyperinflation. May have obstructive pattern on PFT.
“coal workers lung
Caplan syndrome
(RA) and pneumoconiosis that manifests as intrapulmonary nodules,
mining, sand blasting, quarry, stone increase risk TB;
silicosis
silicosis CXR
CXR: multiple small (<10mm) round nodular opacities primarily in the upper lobes. Bilateral nodular densities progress from the periphery to the hilum. + egg shell calcifications of the hilar & mediastinal nodes (only seen in 5%). Lung Biopsy
berylliosis
aerospace, nuclear, ceramics requires chronic steroids; CXR: normal 50%, hilar lymphadenopathy, increased interstitial lung markings.
Byssinosis:
Byssinosis: brown lung diseases, Monday fever, d/t cotton exposure
asbestosis increased risk of CA, mesothelioma; CXR: pleural plaques (pleural
ABG with asthma
respiratory alkalosis* classic with exacerbation
when should you admit a pt for asthma exacerbation
PEFR <50% predicted, AMS
when can you discharge a pt with a asthma exacerbation?
Discharge—>PEFR >70%, improvement for >1 hour
LABA examples
salmetrol, symbicort(budesonide/formoterol) Advair)
improves resp muscle endurance, narrow therapeutic window
Theophylline
heliox works by
decreases airway resistence)
chronic Bronchitis
CXR
increased vascular markings, enlarged right heart border
ECG: cor pulmonale, multifocal atrial tachycardia
emphysema CXR
hyperinflation,
decreased vascular markings
+/- bullae
Tx for COPD exacerbation
Tx: bronchodilators: combo with B2agonist + anticholinergic
B2= albuterol, terbutaline, salmeterol (long acting)
Anticholinergic= tiotropium(Spiriva), ipratropium (atrovent)
when would you use corticosteroids in COPD exacerbation
when would you use theophylline
not monotherapy, may be added to LABA (salmeterol + fluticasone)
when would you use O2 in a COPD exacerbation
Use if cor pulmonale,
02sat <88% or
Pa02 <55mm Hg.
gold standard for TB dx
Acid fast smear & sputum cultures x 3 days (AFB cultures GOLD STANDARD
treatment for latent TB
INH + pyridoxine 9 months (12 mon if CXR granulation or HIV +)
TB treatment for people that have had contact with infected persons
If in contact: RIF + PZA 4 months (consult ID specialist)
treatment for active TB
RIPE
(rifampin, INH, pyrazinamide, ethambutol).
Total tx of active is 6 months (or 3 months after negative sputum culture).
if culture shows sensitivity to INH and RIF —> stop other two
rifampin adverse side effects
Thrombocytopenia,* flu-like symptoms. Orange colored secretions* [ex tears, urine]. GI upset, hypersensitivity, fever, hepatitis.
isoniazid adverse side effects
Hepatitis* (especially >35y ofage). Peripheral neuropathy.*
Drug-induced lupus, rash.
Abdominal pain, high anion gap acidosis. Cytochrome P450 inhibition.____________
MUST TAKE WITH PYRIDOXINE . B6
Pyrazinamide adverse side effects
Hepatitis & hyperuricemia.
GI symptoms, arthritis.
Photosensitive dermatologic rash
etambutol EMB adverse side effects
optic neuritis
red green
3 criteria for latent tB
asymptomatic person
PPD +
No evidence of active infection on CXR or CT (NOT contagious)
why do you use Bronchoalveolar lavage in TB
Bronchoalveolar lavage: used to r/o infectious causes. Sarcoid: incr. CD4:CD8 (increased CD4, decreased CD8)
Tx for sarcoidosis
Oral corticosteroids TOC*
Methotrexate (steroid alternative) watch for toxicity though
Hydroxychloroquine: may be good for chronic disfiguring skin lesions.
NSAIDs for musculoskeletal symptoms & erythema nodosum
Single lung transplant in severe cases.
Ear pain, bullous myringitis*(eardrum), non-productive cough, erythematous pharynx (pharyngitis), URI sx
mycoplasma pneumonia
age <50 years persistent cough dry cough long duration of symptoms Other Factors recent community exposure fever headache diarrhea bullous myringitis lung rales/crepitations throat involvement rash
mycoplasma pneumonia dx
Send serum cold agglutinins for Dx
mycoplasma pneumonia tx
Doesn’t respond to B-lactam, lacks cell wall. Use macrolide
azithromycin : 500 mg orally once daily on the first day, followed by 250 mg once daily for 4 days; 500 mg intravenously once daily for at least 5 days
clarithromycin : 500 mg orally (immediate-release) twice daily for 14-21 days
erythromycin base : 500 mg orally four times daily for 14-21 days; 1000 mg intravenously four times daily for 14-21 days
pickwickian syndrome
obesity hypoventilation syndrome—condition in which severely overweight people fail to breathe rapidly or deeply enough, resulting in low blood O2 and high CO2 levels.
alveolar hypoventilation results from blunted ventilatory drive and increased mechanical load imposed by obesity
can lead to heart failure symptoms
hypoxemia during sleep .
get polysomnography and screen TSH and cbc
HBsAg
Infected
>6 months chonric
1st evidence
HBsAb
vaccination of distant resovled infection
if this doesn’t exist than you can assume chronic infection
HBcAb
if IgM then acute
if IgG than chronic or immune through exposure
HBeAg
increase in viral replication
increased infectivity
charcot’s triad sx
Most patients have fever, jaundice, and right upper quadrant pain (Charcot triad).
biliary colic
occurs after a fatty meal in which the gallbladder contracts and pushes stones into the cystic duct; when the duct relaxes, the stone retreats back into the gallbladder causing visceral pain.
Cholecystitis is..
Cholecystitis—obstruction of the cystic duct resulting in acute inflammation of the gallbladder wall.
Choledocholithiasis is..
Choledocholithiasis—gallstones located in the common bile duct.
cholangitis is ..
gallstones in the ampulla of vater
dx cholestasis aka biliary colic
high alk phos
juanidce
dark urine
cholelithiasis
RUQ ultrasound high sensitivity
(IF >2MM)
can also get MRI or CT
what is boas sign
referred right subscapular pain with cholelithiasis
acute cholecysitis sx
pain lasts days
RUQ
epigastrium
nausea, vomiting, anorexia
MURPHY sign
GET HIDA WHEN ULS inconclusive
will see elevated ALK-Pand GGT
tx for acute cholecysitis
IV fluids bowel rest IV abnx analgesics cholecystecomy within 48 hrs but timing depends on severity
choledocholithiasis
stones in the common bile duct (CBD)
primary:
originate in CBD
secondary: originates in GB passes to CBD
choledocholithiasis sxs
RUQ or epigastric pain
jaundice
NO FEVER
dx test for choledocholithiasis
RUQ ULS first but not sensitive
ERCP -GOLD STANDARD
TX FOR choledocholithiasis
ERCP with sphincterectomy and stone extraction with stent placement
lap choledocholithotomy
can complicate and turn into cholangitis
cholangitis dx tests
infection of biliary tract seocndary to obstruction and bacterial overgrowth
ULS first
ERCP after
blood culture
PSC
ERCP decompression or can progress to hepatic abscess chornic idopathic progressive
disease of intraheptatic or extrahepatic bile ducts
thickening
and narrowing of lumen
liekly triggered by immune mediated bile duct injury (STRONG ASSOCIATION WITH ULCERATIVE COLITIS)
What is the sxs associated with PSC
insidious onset
chronic cholestasis
progressive to jaundice and itching
fatigue
malaise
weight loss
dx test for PSC
ERCP
LFTS
PSC tx
liver transplant
cholestyramine should give sx relief of itching
primary biliary cirrhosis
chronic and progressive cholestatic disease with destruction of intraheptic bile ducts with portal inflammation and scaring
autoimmune
fatigue itching many asxs hyperpigmentation jaundice ascites
need liver biopsy
abdominal ULS to rule out obstruction
primary biliary cirrhosis
symptomatic and transplant
Hemochromatosis
Bronze diabetes
Autosomal recessive
HFE gene
Increased iron storage absorption
MC among Caucasian makes
Progressive iron absorption in the GI tract
Increase deposits in the liver heart,
Pancreases
And pituitary
What sus do you see with hemochromatosis
Liver disease Skin pigmentation DM Arthropathy Impotence Cardiomyopathy
Bets screening test for hemochromatosis
Transferrin saturation
(Values greater than 45%) indicate further testing
Elevated serum ferritin is good evidence over overload
Liver box is gold standard but not needed
Might seem hyperglycmemia
Elevated LFTs
Tx for hemochromatosis
Phlebotomy
Goal to bring ferreting level below 50
The cheating agent deferoxamine has to be given daily as a9-12 hr IV or SC infusion and complaisance is difficult
Oral cheating deferasirox is effective but should not be given in pts with high risk myelodysplastic syndrome because it can cause renal impar EENT, hepatic impairment or GI hemorrhage
Te for pt with diarrhea
Abdominal distensión
And vesicular lesión found on extensor surfaces of arms and legs
Celiacs
Get anti endometrial antibodies or anti trans glutaminase Ab
Bx of small bowel revelas villus and atrophy blunting Megaloblastic anemia (poor folic acid B12 absoption)
Will increase risk of cirrhosis
Vitamin supplementation corticosteroids may be needed in refractory
IBD with watery diarrhea what is the dx test and what would you see
Skip lesions on endoscopy of sigmoid or colonoscopy will reversal cobblestoning appearance
Rectal sparring
Will probably need CT and will show inflammation throughout the bowel wall at the ileso e al junction and mesenterio fat wrapping
Tx Crohn’s
5-ASA mesalmine for maintenance
Prednisone for acute
Metronidazole if not responding to 5 ASA or perineal disease fistula or dfissure
I uno suppressing drugs might be needed like azathioprine or 6-mercaptopurine
Supplement b12 FOLATE Vitamin D
Gold standard dx for pr with epigastric pain
Dyspepsia
Abdominal pain
Get endoscopy
Gastritis tx
If H pylori
NSAIDs empiric therapy with acid suppression
4-8 Wk PPI
If no response then test for H pylori
PPI+ 2 antibiotics for 2 wk or quad therapy
Clarithro+amoxicillin+PPI
(CAP)
Metronidazole if PNC allegory
Flapping tremor
Musty breath
AMS
Te
Hepatic encephalopathy
Lactulose or Rifazimin, lactitol
Neomycin is 2nd line
Protein restriction
RUQ
Jaundice
Fever
MCC and dx
What is the test
Choledocolithiasis is MCC
But cholangitis is the dx
Get ERCP or PTC
Get CBC
Increase in ALK with GGT
Tx of Cholangitis
Antibiotics and ERCP common bile duct decompression
ROME CRITERIA for IBS
BOUTS OF DIARRHEA for at least 3 months
Associated with at least 2 of the following 3
- Related to defecation
- Onset associated with stool frequency
- Onset associated with change in stool form
Improvement with defection
Change in consistency
PP urgency
If no alarm symptoms just reassurance and life style changes
Dx studie for diverticulitis
CT scan increased WBC
Guiac +
Diverticulitis —> inflamed diverticula
Secondary to obstruction/ info.
Fever LLQ pain
N/V/D/C flatulance
Acute cholecysitis dx test
HIDA
Pathophysiology of PUD
Decrease mucosal protective factors
Mucus, bicarbonate, PG, and blood flow
- Increasing damaging factors like acid and pepsin
DU more common than GU
2-5 hrs—> duodenal
1-2 hrs after—> gastric
Copious watery
Non blood diarrhea with flecks of mucus and low grade fever
No fecal orador
Dx test
Rice water stool chokers do rapid dipstick testing
Fluid replacement is mainstay and tetracycline antibiotiotics or FQ or macrolides
Hepatitis d REQUIRES
HEPATITIS b
DX test GERD
Usually endoscopy often used 1st but the gold standard is 24 hour ambulatory pH monitor is GOLD STANDARD
Gastroenteritis when do you use anbx
Travelers diarrhea and SHigella both have bloody stool
ETEC
Give cirpofloxacin
If preganant azithromyocin
SHigella - largest amount of fecal leukocytes
TMP.SMX
Cholera - shellfish rice water—>FQ
MC type of hepatocellular carcinoma
Non-fibrolamellar
Associated with hep B/C
Unresectable with short survival time
Fibromalar is respectable and not seen with HEP, occurs in younger pts.
Get alpha 1 FP and do LR biopsy
diagnostic test for RA
+ rheumatoid factor, +
Anti-citrullinated protein antibodies (ACPAs)
CCP- cyclic citrullinated peptides contian these antibodies
what is the presentation of lumbar stenosis and how does it present
pseudoclaudication, neurogenic
Narrowing of spinal canal impingement of the nerve roots & cauda equine
Back Pain with paresthesias
Worse with extension (prolonged standing/walking)
RELIEVED with flexion (sitting/walking uphill)
Lumbar epidural injection of steroids
worsening of OA
MC in weight bearing joints
Narrowed joint space, sclerosis, osteophyte formation
Evening joint stiffness (worsens throughout the day)
Heberden’s nodes are present on the
Heberden’s nodes
DIP
treatment of OA
Acetaminophen NSAIDS corticosteroid injections
tx of morton’s neuroma
Steroids, wide shoes, surgery if persists
Wide shoes, glucocorticoid injection* , surgical resection leaves patient with perm. Numbness
what tests would you see with polyarteritis nodosa
Increased ESR, ANCA negative
Angiography microaneurysm with abrupt cut-off of small arteries
Steroids
what is polyarteritis nodosa and what are the associated sxs
systemic vasculitis of medium/small arteries –?necrotizing
Ass with hep B & C*
Increased microaneurysms, muscular arteries involved
constitutional symtomns and abdominal pain
HTN, renal failure, neuropathy, livedo reticularis (lungs spared*)
allupurinol should not be given with
Allopurinol reduces uric acid production by inhibiting xanthine oxidase
AVOID DIURETICS!!!
what is pseudo gout
accumulatin of crystals of calcium pyrophosphate dehydrate (CPPD) in connective tissues
chondrocalcinosis
MC location of pseudogout
Knee
polymalgia rheumatica
Idiopathic inflam condition, synovitis, bursitis, tenosynovitis
aching/stiffness of proximal joints, bilateral
difficulty brushing hair, putting on coat, getting out of chair
Hips, shoulder, neck
polymalgia rheumatica has a stonrg association with what other dx
Closely related to Giant cell arteritis
tx for polymyalgia rheumatica
corticosteroids taper after 4-6 weeks stop in 1-2 years
self limiting
what is morton’s neuroma and how do you diagnose it
Painful mass near plantar surface of foot, radiates to 3rd,4th toe, pain on ambulation
Reproduce pain by squeezing foot forcing met heads together
MRI needed for diagnosis
Steroids, wide shoes, surgery if persists
jobes test is for
Jobes test or Empty can test isolated examination of supraspinatus muscle
this muscle from the deltoid
Jobes bring arm up and to the front, with arm internally rotated (thumb to floor), downward force and try to resist the force.
If it drops then could mean rotator cuff tear
MC location for SAH
arterial bleed between arachnoid and pia
MC Berry aneurysm rupture (AVM)
other than worst headache of life what are some common sxs seen with SAH
Stiff neck, photophobia, delirium
worst head of life
what would you do if CT was negative but you suspected SAH
what would you see
LP —> xanthochromia
tx for SAH
Supportive, Bedrest, antianxiety meds
Uhthoff’s phenomenom
MS
Uhthoff’s phenomenom worse with heat
Lhermitte’s sign
neck flexion causes lightning-shock pain from spine to leg
MS
MS diagnosis
increase IgG in CSF (oligoclonal bands)
MRI with gadolinium: MRI test ofchoice in helping to confirm MS.*
long term medications for MS
fi-interferon* or Glatiramer acetate (Copaxone) decrease #/severity of relapses.
guillan barre LP reuslts n
high protein with normal WBC count
This is know n as albuminocytological
dissociation.
May be due to altered neuronal capillary-CSF barrier defect.
RF for Bell’s pa;sy
Diabetes mellitus, pregnancy (esp 3rdtrimester), post URI, dental nerve block.
treatment for guillan barre
what is CI
lasmapheresis best if
done early.
MOA:removes harmful circulating auto-antibodies that
cause demyelination. Equally as effective as IVIG. Patients are usually hospitalized.
DO NOT GIVE PREDNISONE
CNI
olfactory
CN II
optic
VA
PLR
III
oculomotor EOM (inferior rectus, ciliary body)
IV
TROCHLEAR
EOM superior oblique
VI
abducens
lateral gaze
VII
facial motor of the face
VIII
acoutise of vestibulocochlear hearing and balance
IX
glossopharyngeal
taste posterior 1/3 of the tongue
X
Vaguse
gag reflex
voice
soft palate
XI
accessory motor neck and shoulder
XIII
hypoglossal
tongue deviation
fasiculation
decerebrate
arms adducted to side
damage to upper brain stem
E
E
E hands for E extensor
This is 2 points on the GCS
decorticate
arms flexed and on chest damage to corticospinal tract
decor c c c FLEX
THIS IS 3 POINTS ON THE GCS
genetics of huntington’s
what is the pathophysiology
autosomal dominant
neurodegenetive disorder caused by a gene mutation
neurotoxicity as well as cerebral, putamen & caudate nucleus atrophy.
progression of huntington’s disease
r 30-50y ofage. Initial O behavioral => Q chorea* & © dementia.
diagnosis of huntington’s disease
CT
cerebral &
CAUDATENUCLEUSATROPHY.* MRI shows similar findings. Genetic testing.
- PET scan: decreased glucose metabolism in the caudate nucleus & putamen.
symptoms of parkinson’s
tremor
resting pill roll
wrosen at rest and with emotional stress
lessoned with voluntary activity and intention usually confinded to one limg
tx for parkinson’s
if young use dopamine agonists like bromocrptine or more recently ropinarole
can also use anticholinergics like benzotropine in younger pts
if older than 70 go straight to carvidopa levadopa
absolute CI to anticholirgics like trihexyphenadyl and . benzotropine
nstipation, dry mouth, blurred vision, tachycardia, urinary retention. CL BPH, glaucoma.
Selegiline, Rasagiline how do they work
increases dopamine in the striatum (MAO-B normally breaks down dopamine).
how do entacapone, Tolcapone. work
Catechol-O-Methyltransferase (COMT) inhibitors
entacapone, Tolcapone. Adjunctive tx. MOA: prevents dopamine breakdown. Ex. S/E: GI sx, brown discoloration of urine.
sxs of constrictive pericarditis
Dsypnea, Right sided heart failure (JVD during inspiration, periph edema, hepatojugular reflux) , **pericardial Knock (high pitched 3rd heart sound from sudden cessation of ventricular filling from thickened inelastic pericardium)
tx of constrictive pericarditis
Tx: pericardectomy, diuretics (for symptoms)
, Primary aldosteronism sxs
HTN, hypokalemia, hypernatremia, metabolic alkalosis
headaches, flushing of the face.
what is primary hyper aldosteronism
is RenIn-independent (autonomous).
- Idiopathic or idiopathic bilateral adrenal hyperplasia (60%). MC in women.
- Conn’s syndrome:adrenal aldosteronoma*(40%) located in the zona glomerulosa.
Unilateral adrenal hyperplasia (rare).
initial labs if suspecting hyperaldosteronism,
Labs:
Hypokalemia
WITH
METABOLICALKALOSIS*(dueto dumping of K+&H+in exchange for Na+).
if pt has hypokalemia and HTN
what is the workup on this pt
suspect hyperaldosteronism
inital test would be a aldosteron: renin ratio showing >20
then a salt supression (saline infusion) test if non reactive would suggest primary aldosteneronism or conn’s syndrome
then CT MRI
dx and MCC of scrotal pain erythema and swelling
MCC= chlamydia men >35, enteric organism in children & men >35
Scrotal pain, erythema, swelling
dx tests and pysical exam of epidiydimitis
Prehn’s sign (relief of pain with elevation of affected scrotum
US—> increased testicular blood flow, UA—>pyuria or bacteremia
tx for epidyditmitis
Bed rest, scrotal elevation, cool compress, NSAIDs
Gon/chlamydia—> azithromycin & ceftriaxone
Fluoroquinalones
MCC of pyelonephrotos
lower UTI
E. coli, Proteus sp, Klebsiella, Enterobacter sp, pseudomonas
Fever, flank pain, irritative voiding, CVA tenderness
UA of pyelonephritis
UA
pyuria, bacteremia, hematuria, WBC casts
remember this is one of the causes of AIN
outpatient and inpatient treatment of pyelonephritis
Ciprofloxacin, Bactrim (1-2 weeks)
Inpatient—> IV fluoroquinolones, Ampicillin + gentamycin
Then oral ABX 2 weeks after dc
if treatment for pyelonephritis fails
probably obstruction
If fails look for obstruction/abscess
MC organism for UTI
for sexually active women
women MC to have UTI
E. coli MC organism,
staph saprophyticus with sexually active women
dx of UTI
Dx: urinalysis: pyuria (increase WBC (>10 hpf), +leukocyte esterase + nitrates +hematuria)
genetic variations of polcystic kidney disease
cystc replace the mass of kidney, reducing function & leading to kidney failure
AR–> begins in utero, leads to neonatal death
AD–>bilateral
symptoms and sign of PCKD
Back and flank pain, headaches, nocturia
U/S* (fluid filled cysts)
ultrasound ULS
U/S* (fluid filled cysts)
Supportive to ease sxs and prolong life (control HTN, high fluid intake, low-protein diet)
Treatment Polycystic kidney disease
Infections—>Bactrim, fluoro, chloramphenicol, vanco
Dialysis, renal transplant
damage to renal glomeruli by inflammatory proteins in glomerular membranes
focal
Focal—> IgA nephropathy, hereditary nephritis, SLE
damage to renal glomeruli by inflammatory proteins in glomerular membranes
Diffuse—>SLE, vasculitis
signs and sxs of glomerular nephritis
Hematuria, anuria/oliguria, edema of face/eyes/ankles/feet
Steroids, immunosuppressive drugs
control inflame
MC type of bladder cancer and MC risk factor
90% transitional cell (TCC)
smoking MC ris factor
dx of bladder CA made wiht
Dx: cystoscopy with biopsy (diagnostic and curative if able to do excision)
local bladder CA tx
Tx: local–>resection with electrocautery
Invasive bladder CA tx
cystectomy, chemo, XRT
Recurrent bladder CA tx
BCG immune therapy (bacillus Calmette-Guerin)
stage 1 ckd GFR
Stage 1 GFR normal (>90)
Stage 2 CKD GFR
GFR 60-89
Stage 3 GFR
Stage 3 GFR 30-59
Stage 4 GFR
Stage 4 GFR 15-29
Stage 5 GFR
Stage 5 GFR <15 End stage renal failure
presentation of post infectious glomerulonephritis
MC after GABHS*
2-14 year old boys, puffy eyelids, facial edema up to 3 weeks post strep
scanty/cola colored urine (hematuria/oliguria)
dx of glomerulonephritis
increase antistreptolysin titers, low serum complement (C3)
tx of post stre glomerulonephritis
Tx: supportive, antibiotics
FIND THIS OUT
If you have a supraspinatus injury, what ROM will have pain?
Anatomical landmark of upper vs lower GI bleed
Anatomical landmark of upper vs lower GI bleed- ligament of Treitz
Auer rods
Auer rods are AML
MC adult leukemia
CLL is most common adult leukemia
What do you do for asystole?
What do you do for asystole? Shock, unsynchronized
What type of cell is affected in peptic ulcer disease?
What type of cell is affected in peptic ulcer disease?
holosystolic low pitch blowing murmur, heard best at apex, radiation to the axilla
Mitral regurgitation
Wolff-Parkinson-White syndrome
Electrical signals bypass AV node
short PR interval and wide QRS from DELTA WAVES
Myocardial infarction
STEMI:
1) reperfusion* (PCI within 90 minutes or thrombolytic–>TPA (alteplase, streptokinase)
2) antithrombotic (aspirin, heparin)
3) adjunctive (ACE-I*, b-blockers, nitrates, morphine, statin)
-new onset LBBB considered STEMI equivalent
NSTEMI: 1) anti-thrombotic (aspirin, heparin, ADP-inhibitors, GP IIb/IIIa inhibitors, X in)
2)adjunctive (b-blockers, nitrates)
how do you diagnose Prinzmetal angina
coronary angiogram w injection of provocative agents (ergonovine)
ST elevation only tracked while experiencing attack
why you provac it
what is the difference between HFrEF and congestive heart failure
with LVEF ≤40 percent, known as HFrEF
Congestivedecompensated heart failure with worsening baseline
MCC of mitral stenosis
MCC rheumatic heart disease
mitral stenosis leads to
Right sided heart failure, pulm htn, A-Fib, mitral facies (flushed face)
sxs of dilated cardiomyopathy
AKA congestive HF
increased JVD
narrow pulse pressure
pulmonary rales, hepatomegaly,
peripheral edema
S3 and S4
mitral regurg, tricuspid regurg (less common)
echo for dilated cardiomyopathy will show
Echo
LV dilation, high diastolic pressure, low cardiac output
Tx for diastolic HF
Tx:
abstinence from alcohol,
ACE-I,
diuretics (spironilactone)
digoxin (NO MORTALITY)
B-blockers Only carvedilol, long-acting metoprolol succinate, and bisoprolol have shown
. Elsevier Health Sciences. Kindle Edition.
salt restriction
what is venous insufficiency and how does it present
Vascular incompetency of either deep and/or superficial veins
Superficial thrombophlebitis, DVT or trauma
Leg pain (improves with elevation/walking), leg edema, stasis dermatitis, brownish hyperpigmentation, ulcer (medial malleolus), atrophie blanche
MCC of pericarditis
Inflammation of pericardium
Persistent, pleuritic, postural (better sitting/leaning forward), pericardial friction rub
MCC–>viral (enterovirus coxsackie, echovirus)
pericarditis can lead to
Leads to pericardial effusion—>tamponade (pericardiocentesis*)
anterior wall
V1-V4, LAD
lateral wall
V5, V6, aVL, circumflex
Anterolateral
- aVL, V4, V5,V6, LAD or circumflex
Inferior
- II, III, aVF, RCA
Posterior
ST depression V1, V2
diagnosis of LVH
Echo–> asymmetrical wall thickness (septal) >15 mm, systolic anterior motion of mitral valve
EKG–> LVH
tx of LVH
Tx: b-blockers* first line, surgical, alcohol septal ablation(ethanol)
EKG
Amplitude of largest R or S in limb leads ≥ 20 mm = 3 points
Amplitude of S in V1 or V2 ≥ 30
mm = 3 points
Amplitude of R in V5 or V6 ≥ 30 mm = 3 points
dressler’’s syndrome usually occurs how soon after an MI
Pericarditis 2-5 s/p MI
Chest pain (pleuritic), persistent, postural (worse lying down), fever, pericardial friction rub
EKG: diffuse ST elevations
Tx: aspirin or cochicine
restrictive cardiomyopathy aka
restrictive cardiomyopathy
H/O amyloidosis, hemachromatosis, sarcoidosis, fibrosis, ca
what are the diagnostic tests for restrictive cardiomyopathy
ECG–> nonspecific with ST seg and T wave abnormalities
Echo–> diated atria and myocardial hypertrophy
CXR–>coronary vascular congestion (normal heart size)
dx work up of
40 yr old man with clubbing of the fingers bi basilar crackles +/- cyanosis non productive cough
decreased lung volume, honeycombing, ground glass opacities
bx: honeycombing (large cystic airspaces)
CXR/CT scan: diffuse reticular opacities (honeycombing),* ground glass opacities. Biopsy: honeycombing (large cystic airspacesfrom cysticfibrotic alveolitis).
PFT: decreased lung volumes decreased TLC, RV
Red maculopapular rash on wrists and ankle
Red maculopapular rash on wrists and ankles central 2-3 days (face spared)
Rickettsia rickettsia, dog tick, 2-14 days post bite
when do you see RMSF
Red maculopapular rash on wrists and ankles–> central 2-3 days (face spared)
can present with seizure
Fever + rash + h/o bite (camping, trip)
DX of RMSF
Clinical diagnosis (don’t wait for serologies) - fever, rash, history of tick bite.
Serologies: indirect immunofluorescent antibody test for IgM and IgG antibodies
CSF: low glucose & pleocytosis (increased cell count).
mnmgt RMSF
doxycycline–> even in kids
chloramphenicol 2nd line –> PREGNANCY
reaction sixe TB
> 5 IC
10 all other high risk populations
15 everyone else
tetanus dx and management
Neurotoxin blocks neuron inhibition—> severe muscle spasm
Blocks the release of ACH
mgmt: metronidazole
gram-negative rod transmitted via contaminated food & water. Outbreaks may
occur during poor sanitation & overcrowding conditions (especially abroad).
what is the management
cholera
- Supportive:fluid replacement mainstay.* Often self-limited.
- Antibiotics: tetracyclines,
fluoroquinolones or macrolides may shorten the disease course in
patients who are severely ill, other comorbid conditions or with high fever.
most sensitive test for VZV
PCR most sensitive test for VZV
Vesicles on an erythematous base “dew drops on a rose petal”
treat symptoms
Most are asymptomatic (often incidental finding of leukocytosis on routine blood testing], 2. Fatigue MC, dyspnea on exertion, (infections. Lymphadenopathy, hepatosplenomegaly.
Dx: peripheral smear (well-differentiated lymphocytes with scattered SMUDGE CELLS*)
(fragile B cells that often smudge during slide preparation]. Lymphocytosis >20,000/pL.
Pancytopenia: thrombocytopenia, anemia.
MCV >115 almost exclusively seen in …..
especially if hypersegmented neutrophils* arepresent
MCV >115 almost exclusively seen in B12 or Folate deficiency
cobalamine
When replacing the B12 need to check for
Watch for hypokalemia* (replacement leads to cells taking up large amounts of potassium)
Watch for hypokalemia–> replacement leads to reticulocytosis with new cells taking up large amounts of potassium
<3.5, muscle cramps, constipation
flat T waves, U waves
ekg of pericardial effusion
low voltage QRS, electrical alternans
Painful, loss of vision, N/V/diaphoresis
PE: “steamy cornea”, fixed-mid-dilated pupil, decreased visual acuity, injected
tx
TX: immediate referral*, IV carbonic anhydrase inhibitor (acetazolamide)
Classic: come in with stab wound, now hypotensive, distant heart sounds and increased
JVP, narrow puse pressure, pulsus paradoxus…..
Cardiac tamponade
Echo** test of choice diastolic collapse of cardiac chambers*
“water bottle heart” on CXR
EKG: electrical alternans
cardiac tamponade tx
IV fluids to improve hemodynamics, pericardiocentesis* (diagnostic and therapeutic)
post-op with tachypnea
Pulmonary embolism
staus epilepticus tx
Airway—>hyperthermia (cooling blanket)
IV diazepam/lorazepam (until stops)
phenytoin/fosphenytoin
2nd Type I(Wenckenbach) tx
observe, atropine, epi
a-fib tx
RATE control*, vagal, CCB, BB, rhythm- DCC, digoxin
prevent stroke warfarin, aspirin
CMV sxs
Primary disease: most asymptomatic. Mononucleosis-like illness* (if symptomatic).
RETINITIS
ESOPHAGITIS
mostly in IC
CMV retinitis
hemorrhage with soft exudates: scrambled eggs/ketchup appearance (pizza pie)*
appearance on funduscopy if CD4 <50;* Pneumonitis, Encephalitis; Colitis (CD4 <100).
dx of MCV
serologies (Antigen tests, IgM, IgG titers).
PCR.
Biopsy of tissues: Owl’s eye* appearance (epithelial cells with enlarged nuclei surrounded by
clear zone & cytoplasmic inclusions).
tx of CMV
Ganciclovir* treatm ent o f choice. 2 nd line: Foscarnet, Cidofovir. Valacyclovir.
tx for toxoplasmosis
Sulfadiazene (or Clindamycin) + Pyrimethamine (with folinic acid/leucovorin to prevent bone marrow suppression & reduce nephrotoxicity). Spiramycin if pregnant.
sxs of gonococcal urethritis
brupt onset of symptoms (especially within 3-4 days). Opaque, yellow,
white or clear thick discharge, pruritus. Up to 20% of patients are asymptomatic.
posterior electrocardiogram (C) would be appropriate to evaluate for posterior ST segment elevation if you saw
osterior electrocardiogram (C) would be appropriate to evaluate for posterior ST segment elevation if you saw deep depression in leads V1 and V2 with prominent R waves.
what ECG findings are suggestive of an inferior wall infarct. This patient is suffering from hypotension and bradycardia as well, which suggest a potential right ventricular infarct
ST segment elevation in leads II, III, and aVF is suggestive of an inferior wall infarct. This patient is suffering from hypotension and bradycardia as well, which suggest a potential right ventricular infarct
Which of the following is the treatment of choice in antidromic atrioventricular reciprocating tachycardia in a hemodynamically stable patient?
Procainamide
