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5 star topics Flashcards

1
Q

Valves open during systole

A

Aortic, pulmonic

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2
Q

Valvular lesions producing systolic murmurs

A

MR, TR, AS, PS, Mitral valve prolapse

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3
Q

Valves open during diastole

A

mitral, tricuspid

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4
Q

Valvular lesions producing diastolic murmurs

A

MS, TS, AR, PR

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5
Q

Murmurs and sounds heard best with patient in left lateral decubitus position

A

Mitral murmurs

Left sided S3, S4 heart sounds

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6
Q

Cardiac auscultation findings considered benign when there is no evidence of disease

A

Split S1
Split S2 on inspiration
S3 under 40 yo
early, quiet systolic M

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7
Q

Causes of aortic stenosis

A

Congenital bicuspid valve - about 40 yo
Senile calcifications - over 60 yo
Rheumatic heart disease
Tertiary syphilis - aortitis (tree barking of aorta and dilation of aortic root -> AS, AR, dissection)

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8
Q

Presentation of aortic stenosis

A

Dyspnea (CHF)
Syncope
Angina
-all with exertion

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9
Q

Physical exam findings with aortic stenosis

A

Ejection click
Systolic ejection murmur “crescendo-decrescendo” heard at RUSB
Murmur radiates to neck/carotids

Valsalva will decrease the murmur

Peripheral pulses are weak and prolonged/delayed “pulsus parvus et tardus”

Next step: ECHO

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10
Q

Treatment of aortic stenosis

A

aortic valve replacement if symptomatic

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11
Q

Causes of Mitral regurgitation

A 
MV prolapse
Rhematic heart disease
infective endocarditis
papillary muscle rupture
LV dilation (from ischemic heart disease or dilated cardiomyopathy)
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12
Q

Presentation of MR

A

often asx
Fatigue
Exertional dyspnea
A fib with LA dilation

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13
Q

Physical exam findings of MR

A

holosystolic murmur heard at apex, may radiate to axilla

Next step ECHO

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14
Q

Treatment of MR

A

Vasodilators for LV dysfunction
Anticoagulate patients with Afib or hx of rheumatic heart disease
Mitral valve repair

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15
Q

Mitral valve prolapse

A

Large billowy leaflets into atrium

Midsystolic click with late systolic crescendo murmur

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16
Q

Causes of aortic regurgitation

A

Infective endocarditis
Rheumatic heart disease
Tertiary syphilis - aortitis (tree barking of aorta and dilation of aortic root -> AS, AR, dissection)

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17
Q

Presentation of Aortic regurgitation

A

usually asx until severe

Dyspnea, heart failure

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18
Q

Physical exam findings of aortic regurgitation

A

Wide pulse pressure - normal SBP, DBP way off
Bounding pulses
de Musset sign - rhythmic bobbing of head
Rumbling, early diastolic murmur heard at RUSB or Left side of sternum

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19
Q

Treatment of aortic regurgitation

A

Medical management of HF - ACE-i, Bb, spironolactone

Aortic valve replacement

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20
Q

Causes of mitral stenosis

A

Mainly rheumatic heart disease

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21
Q

Presentation of mitral stenosis

A

Dyspnea and CHF - may be exacerbated by pregnancy 2/2 expended blood volume, increased HR and SV -> increased CO

Afib d/t dilation of LA

Most patients have concomitant mitral and/or tricuspid regurgitation

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22
Q

Physical exam findings of mitral stenosis

A

Opening snap after S2

Rumbling, late diastolic murmur at apex

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23
Q

Treatment of mitral stenosis

A

Balloon valvuloplasty

diruetics for CHF sxs prior to valvulopasty
Anticoagulation pts with Afib

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24
Q

Presentation of shock

A 
Hypotension
\+/- tachycardia
\+/- cool, clammy, cyanotic skin
Decreased urine output - monitor closely
AMS - monitor closely
Metabolic acidosis - d/t anaerobic metabolism - check lactic acid level and BMP for anion gap
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25
Mechanisms, causes, and treatment for Hypovolemic shock
Mech: decreased intravascular volume Cause: hemorrhage - trauma, GI bleed; burns; GI losses - prolonged V/D Tx: IVF, blood transfusion, tx underlying cause
26
Mechanisms, causes, and treatment for Cardiogenic shock
Mech: pump failure Cause: acute MI, dilated CM, arrhythmia, ruptured septum, papillary muscle rupture Tx: Dobutamine (beta 1 effect); intra-aortic balloon pump Caution IVF can lead to pulmonary edema
27
Mechanisms, causes, and treatment for Obstructive shock
Mech: Extracardiac causes of pump failure; decreased venous return and decreased preload Cause: Tension PTX -> decreased preload; hemothorax; PE; cardiac tamponade Tx: Tx underlying cause; pericardiocentesis for tamponade; chest tube for PTX
28
Mechanisms, causes, and treatment for Septic shock
Mech: peripheral VASODILATION due to infection Cause: infection Tx: IVF, NE if IVF fails, Abx
29
Mechanisms, causes, and treatment for Anaphylactic shock
Mech: peripheral VASODILATION due to severe type 1 hypersensitivity reaction Cause: allergic reaction Tx: Epi - vasoconstrict, increase CO = increased BP, airway dilation; IVF; airway management - O2, ET; diphenhydramine, H2 blocker
30
Mechanisms, causes, and treatment for Neurogenic shock
Mech: peripheral VASODILATION and BRADYCARDIA due to autonomic dysregulation Cause: CNS injury Tx: IVF, vasopressors, atropine for brady
31
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for hypovolemic shock
MAP - low - hypotension SVR - increased HR - increased PCWP - low PCWP after fluid challenge: unchanged or increased
32
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for cardiogenic shock
MAP - low - hypotension SVR - increased HR - variable PCWP - increased PCWP after fluid challenge: higher, not volume issue
33
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Obstructive shock d/t lung cause (tension PTX, hemothorax, PE)
MAP - low - hypotension SVR - increased HR - increased PCWP - low or normal PCWP after fluid challenge: unchanged or increased
34
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Obstructive shock d/t cardiac tamponade
MAP - low - hypotension SVR - increased HR - increased PCWP - increased PCWP after fluid challenge: increased
35
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Septic shock
MAP - low - hypotension SVR - low - vasodilation HR - increased PCWP - normal PCWP after fluid challenge: increased
36
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Anaphylactic shock
MAP - low - hypotension SVR - low - vasodilation HR - increased PCWP - normal PCWP after fluid challenge: increased
37
Hemodynamics (MAP, SVR, HR, PCWP, PCWP after fluid challenge) for Neurogenic shock
MAP - low - hypotension SVR - low - vasodilation HR - increased PCWP - normal PCWP after fluid challenge: increased
38
Normal PR interval
conduction delay through AV node | less than 1 large box (200 ms)
39
P wave
atrial depolarization
40
QRS
ventricular depolarization normal 3 small boxes - less than 120 ms = narrow
41
ST segment
ventricles depolarized
42
T wave
Ventricular repolarization Peaked - hyperkalemia flat - hypokalemia
43
U wave
papillary or purkinje repolarization prominent in hypo/hyperkalemia, hyperthyroidism
44
First degree block
PR greater than 0.2sec (large box) Causes: AV node disease, increased vagal tone, drugs increasing refractory time of AV node (b-blockers, CCB, digoxin) Tx: usually asx, not needed
45
Second degree Mobitz type I block (Wenckebach)
Progressively lengthened PR interval until blocked QRS occurs then resets normal, athletes, older, other heart dz Causes: AV node disease, drugs Tx: adjust medications, pacemaker for symptomatic bradycardia - usually asx
46
Second degree Mobitz type II block
Cause: infra nodal conduction problem - bundle of His, Purkinje fibers randomly blocked QRS without PR interval changes Can progress to third degree AV block Tx: pacemaker - usually asx
47
Third degree block
Absence of conduction between atrium and ventricles Dizziness, syncope, hypotension Avoid B-blockers, CCB, digoxin Tx: ventricular pacemaker
48
Paroxysmal supraventricular tachycardia
HR >100, arising from atria or av junction Narrow QRS D/t re-entry anomaly young patients - palpitations - CP - sudden tachy - SOB - syncope Tx: carotid massage, valsalva, IV adenosine, CCB, B-blocker, cardioversion, catheter ablation
49
Multifocal atrial tachycardia (MAT)
supra ventricular origin Older patients - COPD exacerbations Several foci initiating signals -> P waves with variable morphology, at least 3 different Tachycardia Tx: CCB - verapamil, diltiazem; b-blockers, correct hypokalemia above 4, correct hypomagnesemia over 2, catheter ablation
50
Bradycardia
less than 50 ppm (up to 60) Caused by increased vagal tone or nodal disease MC: elderly, hx of CAD, b-blockers, CCB asx or weakness, syncope, fatigue Tx: stop precipitating medications, pacemaker - sxs frequent or severe
51
AV nodal re-entry
fast and slow conduction system at AV node | Fast goes quick to ventricles and retrograde through slow pathway to AV node -> conduction loop
52
AV re-entry (WPW syndrome)
separate accessory conduction path MC - Bundle of Kent Return to AV node WPW associated with delta wave - upstroke prior to QRS -tachycardia, narrow QRS
53
Common causes of upper GI bleeding
proximal to the ligament of trietz MC: PUD - gastric more likely to bleed than duodenum Esophagitis Esophageal varices Mallory-Weiss tears Gastritis Gastric/duodenal cancers
54
Common cases of lower GI bleeding
Distal to ligament of trietz Vascular malformations - angiodysplasia, AVM mesenteric ischemia Meckel's diverticulum (secretes gastric acid) Colon CA Diverticular disease UC Hemorrhoids
55
Signs of Upper GI bleed
hematemesis - ongoing coffee ground emesis melena +/- BRBPR - laxative effect
56
Signs of lower GI bleed
hematochezia - rapid or heavy BRBPR Melena
57
Hemodynamic instability
S/S: hypotension, tachycardia Start IVF right away Substantial loss -> anemia Can have stable Hct d/t loss of both RBC and plasma
58
Steps in management of acute upper GI bleed
assess hemodynamic stability Admit to ICU - NPO Type and screen 2 units RBC Labs: CBC, PT/PTT, BUN, Cr - hypovolemic/reabsorption of bili elevates BUN -> >20:1 -give FFP if PT/PTT elevated If bleeding source uncertain consider NG lavage Medications: IV PPI If variceal bleeding - octreotide - decreases splanchnic blood flow to GI tract EGD
59
Steps in management of acute lower GI hemorrhage
Assess hemodynamic stability - usually stable Type and screen 2 units of PRBCs Labs: CBC, PT/PTT, BUN, Cr NG lavage and/or EGD to r/o massive upper GI bleed prn Colonoscopy up to terminal ileum -if not diagnostic or not feasible - too much bleeding and bleeding persists -> -angiogram (AVM) -Radionuclide scan - "tagged RBC scan" to localize to quadrant -Capsule endoscopy
60
Main risk factors for colorectal cancer
adenocarcinoma ``` Adenomatous colon polyps hereditary syndromes FHx of colon cancer Previous colon cancer UC > Crohns AA - younger Low fiber/high fat diet etOH Smoking DM ```
61
Familial adenosis polyposis
Hundreds of adenomatous colon polyps - shag carpet Mutation Adenomatous Polyposis Coli (APC) gene ``` tumors: stomach/duodenal polyps osteomas fibromas lipomas medulloblastomas ``` Tx: ppx subtotal colectomy before 25
62
Hereditary nonpolyposis colon cancer (HNPCC) aka Lynch syndrome
cancers arise from basically normal appearing colonic mucosa - not polyps cancers develop early 40s-50s Cancers form in proximal colon - right side
63
Peutz Jegher's syndrome
hamartomas in GI tract | Pigmented lesions on lips and oral mucosa
64
Colon cancer screening guidelines
Average risk: - start t 50 yo colonoscopy q10 yr Flex sig q 5 yr Fecal occult blood test annually CT colonography if positive -> colonoscopy Screening stops when patient's life expectancy is less than 5 years or age 75 whichever comes first If polyps - screen 3-5 yr with colonoscopy FHx - age 40 or 10 yr before age of family member
65
S/S of colon cancer
GI bleeding: hematochezia - left sided cancer Melena - right sided cancer Iron def. anemia Change in stool caliber - left sided -pencil thin or flat ribbon like Bowel obstruction - constipation, abdominal distension, N/V Apple core lesion on barium enema
66
Staging colon cancer
CT chest, abd, pelvis No LN involvement - stage I, II -> resect Regional LN involved - Stage III -> resect, adjuvant chemo Distant mets - IV -> palliative chemo MC mets - liver, lung MC chemo - 5-FU
67
Post-treatment surveillance for colon cancer
CEA - q3-6 mo for at least 3 years CT Chest/Abd q1 yr for at least 3 years - pelvis iv rectal CA Colonoscopy at 1 yr, then q3-5 yr depending on findings
68
``` Iron deficiency anemia iron studies Serum iron Transferrin (TIBC) % transferrin saturation Ferritin ```
Serum iron low Transferrin (TIBC) high % transferrin saturation low less than 12 % Ferritin low
69
``` Anemia of chronic disease Serum iron Transferrin (TIBC) % transferrin saturation Ferritin ```
Serum iron low Transferrin (TIBC) low normal % transferrin saturation normal >18% Ferritin normal or high
70
``` Lead poisoning Serum iron Transferrin (TIBC) % transferrin saturation Ferritin ```
Serum iron normal or elevated Transferrin (TIBC) normal of low % transferrin saturation normal Ferritin normal or high
71
``` Sideroblastic anemia Serum iron Transferrin (TIBC) % transferrin saturation Ferritin ```
Serum iron high Transferrin (TIBC) low % transferrin saturation normal or high Ferritin high
72
``` Hemochromatosis Serum iron Transferrin (TIBC) % transferrin saturation Ferritin ```
Serum iron high Transferrin (TIBC) low % transferrin saturation high Ferritin high - if normal r/o hemochromatosis
73
``` Thalassemia Serum iron Transferrin (TIBC) % transferrin saturation Ferritin ```
Serum iron normal or high Transferrin (TIBC) normal % transferrin saturation normal Ferritin normal or high
74
Tension headache
MC type of headache Associated with fatigue and stress Typically bilateral, band squeezing Frontal or occipital location, may involve neck No aura, photophobia, phonophobia, or nausea/vomiting no testing Tx: NSAIDs Second line: dihydroergotamine or sumatriptan -vasoconstrictors - avoid in CAD, Prinzmetal angina, pregnant
75
Migraine headache
Young adult female Triggered by: fluctuations in estrogen, OCP's, tyramine or nitrate rich foods (chocolate, cheese, processed meats, aged foods, old bananas) Throbbing unilateral headache Nausea/vomiting Photophobia and/or phonophobia Visual aura - streaks of light or blurring (increased risk of stroke) ``` Tx: Mild: NSAID or acetaminophen Mod-Sev: -PO tryptan (sumatripin) + naproxen Dihydroergotamine (DHE 45) Antiemetics - chlorpromazine, prochlorperazine, metoclopramide ```
76
Migraine prophylaxis
``` TCAs - amitriptyline, nortriptyline B-blocker - propranolol, metoprolol Anticonvulsant - valproic acid, topiramate, gabapentin Verapamil Naproxen ```
77
Cluster headache
Young male smokers Headache occurs same time daily for weeks, may stop for several months Severe unilateral periorbital headache Conjunctival injection Lacrimation Nasal congestion +/- nasal discharge Partial Horner syndrome - ptosis and miosis without anhydrosis Tx: 100% O2 - 6+L/min on nonrebreather for 20+ min Sumatriptan (or other triptan) Dihydroergotamine (DHE 45)
78
Headache features suspect of brain tumor
Mild headache progressively worsening over days to weeks New onset after age 50 Papilledema Associated seizures, confusion, altered mental status Abnormal neurologic signs and symptoms - numbness, weakness Disturb sleep or presents immediately upon awakening Vomiting proceeds headache known systemic illness - cancer, HIV, or collagen vascular disorder
79
idiopathic intracranial hypertension (IIH)
Young obese female Daily pulsatile headache - worse at night or early morning Nausea/vomiting Retroocular pain worsened by eye movement Papilledema and elevated ICP Most worrisome sequelae is vision loss CT normal CSF: elevated pressure (over 200 in nonobese, over 250 in obese) ``` R/O other pathology with CT and MRI DC inciting agents - excess Vit A, Accutane, long term tetracyclines Weight loss acetazolamide - first line Invasive treatment options: Serial LP Optic nerve sheath decompression Lumboperitoneal shunting - CSF shunt ```
80
Trigeminal neuralgia
Compression of the trigeminal nerve root Lightning like unilateral facial pain Worsened by any stimulation Not associated with neurological defects Carbamazepine - first line Other options: oxcarbazepine, lamotrigine, baclofen Surgical decompression or rhizotomy
81
Epidural hematoma
Laceration of middle meningeal artery Presentation: Trauma -> lucid interval -> lethargy, confusion, or obtundation Headache Vomiting People abnormalities Focal neurological deficits - hemiparesis, seizures CT head w/o contrast - biconvex (Lens shaped) hematoma Avoid LP - risk herniation Tx: Lower ICP - elevate head of bed to 30, hyperventilate, mannitol Craniotomy to drain hematoma
82
Subdural hematoma
Rupture of bridging veins Presentation: Headache - gradually worsens over days to weeks Mental status changes somnolence CT w/o contrast - Crescent shaped hematoma Tx: Craniectomy and surgical drainage - if deteriorating Supportive care monitoring - if stable
83
Subarachnoid hemorrhage - presentation causes
Causes: Rupture of arterial saccular aneurysm - berry aneurysm -Assoc with ADPKD and Ehler's Danlos -MC location - anterior communicating a. and posterior communicating a. Rupture of AVM Trauma Presentation: "worst headache of my life" - thunderclap, sudden Preceded by sentinel headache - severe recurrent headaches in weeks prior to major hemorrhage Neck pain, nausea/ vomiting, +/- fever CT w/o contrast - blood in CSF LP - bloody -Xanthochromia (yellow CSF) - recent bleeding MRA or angiography to identify site of bleeding
84
Subarachnoid hemorrhage - management
Stop all anticoagulants, reverse anticoagulation Keep SBP less than 150 if cognitive function intact until aneurysm is clipped or coiled to prevent replating - if cerebral perfusion not adequate, lowering BP Will increase risk of infarction - Labetalol preferred - avoid nitroprusside and nitroglycerine - can increase ICP Nimodipine (CCB) - prevent vasospasm Prevent physiologic derangements that may worsen brain injury: - avoid hypoxia and hyperglycemia - maintain normal pH, euvolemia and normothermia Definitive treatment: surgical clipping/ coiling
85
Parenchymal brain hemorrhage
MC caused by hypertension Brain tumors, AVMs, anticoagulation Drugs- cocaine, amphetamines ``` Presentation: Focal motor/sensory deficits Headache Nausea/vomiting Seizures Mental status changes ``` CT w/o contrast - bleeding within brain parenchyma MRA or CTA - identify site of bleed ``` Tx: Supportive Control ICP Maintain SBP less than 200 Surgical decompression only for large hemorrhages with elevated ICP to prevent uncal herniation ```
86
Major risk factors of breast cancer
``` Female FHx BRCA 1/2 Estrogen exposures -early menarche -late menopause -fewer pregnancies -less time breastfeeding -older age at first live birth Obesity Advanced age ```
87
Clinical features suggesting breast cancer
``` Fixed, immobile breast mass Peau d'orange New nipple retraction Dimpling Axillary LAD MC - upper outer quadrant ``` Mammo - hyperdense regions and/or microcalcifications
88
Most common sites of breast cancer mets
bone, liver, lungs, brain
89
Ductal carcinoma in situ
arises from ductal hyperplasia Malignant cells fill the duct lumen but do not penetrate the BM eventually -> invasive ductal carcinoma Tx: lumpectomy +/- radiation consider mastectomy in high risk
90
Lobular carcinoma in situ
Arises from lobules but does not penetrate BM LCIS high risk for invasive cancer than DCIS ALWAYS ER and PR positive (more treatable) Tx: observation + tamoxifen if low risk of invasion, no change in survival consider ppx b/l mastectomy
91
Invasive ductal carcinoma
75-80% arises from ducts, penetrates the BM, invades adjacent tissue Rock-hard breast mass with sharp margins, fixed, immobile Stellate border on mammo or bx Tx: early focal - lumpectomy and radiation Multifocal - mastectomy Sentinel LN bx Mets or large tumor >1 cm - chemo
92
Invasive lobular carcinoma
arises from breast lobule and invades adjacent tissue - less fibrotic response often multifocal and/or b/l Slower growing, slower to met Signet ring cells or single-file rows of cells Tx: early focal - lumpectomy and radiation Multifocal - mastectomy Sentinel LN bx Mets or large tumor >1 cm - chemo
93
Inflammatory carcinoma
invasion of dermal lymphatics -> inflammatory changes erythema, wamth, pain, peau d'orange, nipple retraction, dimpling Rapid growing, poor prognosis mimics mastitis - often treated for first and refractory
94
Signet ring cells
Kruckenburg tumors - GI adenocarcinoma - mets to ovary | Invasive lobular carcinoma
95
Paget disease of breast
form fo ductal carcinoma - malignant cells infiltrate the epidermis Eczema-like patches on nipple and areola may indicate underlying cancer in breast parenchyma Bx: cells interspersed - surrounded by clear halo Mammo/US -> bx
96
Treatment considerations in breast cancer
ER and PR positive - treat with tamoxifen Over expression of HER2 - treat with trastuzumab (herceptin) - get baseline ECHO - causes reversible cardiotoxicity BRCA mutations - b/l ppx mastectomy and oophorectomy recommended -60-80% risk of cancers
97
ddx for p-ANCA
eosinophilic granulomatosis with polyangiitis Pauci immune rapidly progressive glomerulonephritis microscopic polyangiitis ulcerative colitis primary sclerosing cholangitis (PSC)
98
Physiologic jaundice
Increased RBCs at birth and fragile fetal RBCs -> increased heme breakdown and increased bilirubin Natural deficiency of UDP glucuronosyltransferase -> decreased conjugation of bilirubin Increased enterohepatic circulation of bilirubin Bilirubin rises between 48-96 hours to 7-9 decreases around day 10
99
Breast milk jaundice
enzyme in breast milk increased intestinal absorption of bilirubin bilirubin does not go down after 2 weeks
100
breastfeeding failure jaundice
Not feeling well or not producing milk Baby dehydrated No bowel movements -> no bilirubin excreted in bile
101
Hemolytic disease causing hyperbilirubinemia
Isoimmune-mediated hemolysis - ABO or Rh incompatability Maternal antibodies attack fetal RBCs causes hemolysis More severe hyperbilirubinemia -> kernicterus
102
Treatment of hyperbilirubinemia
benign causes - no treatment, correct feeding issues Pathologic: phototherapy - converts bilirubin to lumirubin IVIG for ABO or Rh incompatability Exchange transfusion
103
Crigler-Najjar types 1 and 2
Type 1 - no activity of UDP glucuronosyltransferase, needs phototherapy and liver transplant Type 2: milder - no treatment or phenobarbital to stimulate UDPGT
104
Gilbert syndrome
Decreased production of UDP glucuronosyltransferase Jaundice during times of stress No Treatment
105
Biliary atresia
No bilirubin excretion | conjugated hyperbilirubinemia
106
Characteristics of Pathological newborn jaundice
Any jaundice in the first 24 hours Rising total bilirubin by more than 0.5/hr Rise in total bilirubin more than 5/day Direct (conjugated) bilirubin >20% of total bilirubin or >1.5 Total bilirubin higher than 13 in term neonates Jaundice appearing after 2-3 weeks of age
107
Diagnostic criteria for major depressive disorder
At least 5 of 9 in 2 weeks with impaired ability to function: 1 of these required: Depressed mood Interest diminished "anhedonia" ``` Guilt or worthlessness Sleep disturbance Concentration impairment Appetite or wt changes Psychomotor agitation or retardation Energy loss (fatigue) Suicidal ideation (recurrent thoughts of death) ``` "DIGSCAPES"

DIT Level 2 (49 decks)

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