Diseases Quiz 1 Flashcards

1
Q

Strep viridans subacute infectious endocarditis

A

Catalase -; alpha-hemolytic; bacitracin resistant

Most common cause of community caused subacute endocarditis

Most often affects the mitral and aortic valves

Signs and sx: fever, anemia, arrhythmias, abdominal pain, petechiae, septic emboli, Roth’s spots, splinter hemorrhages, and splenomegaly.

Duke Criteria (2 major; 1 major and 3 minor; or 5 minor)

Major = positive blood culture (2 draws); evidence of endocardial involvement

Minor = fever; positive blood culture (1 draw); immunological evidence (i.e. roth spots, osler’s nodes, rhematoid factor); vascular phenomenal (arterial emboli, janeway lesions), and predisposition.

Site of infection is generally through mouth (dental procedure)

Rx: 1.) Ampicillin + sulbactam + gent/tobra
2.) Vanco + ceftri or gent/tobra

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2
Q

Staph Aureus Acute Infectious Endocarditis

A

Gram +, catalase +, coagulase +, facultative anaerobe,

Virulence factors: biofilms, capsule, adhesins, and pathogenicity islands which contain info for methicillin resistance. Protein A (binds FC portion of IgG, coagulase, hemolysins and leukocidins, hylauronidase, staphylokinase, lipase.

Most common cause of nosocomial and IV drug user endocarditis

Signs and sx: fever, anemia, arrhythmias, abdominal pain, petechiae, septic emboli, Roth’s spots, splinter hemorrhages, and splenomegaly.

Duke Criteria: (2 major; 1 major and 3 minor; or 5 minor)

Major = positive blood culture (2 draws); evidence of endocardial involvement

Minor = fever; positive blood culture (1 draw); immunological evidence (i.e. roth spots, osler’s nodes, rhematoid factor); vascular phenomenal (arterial emboli, janeway lesions), and predisposition.

Rx: 1.)Nafcillin/dicloxicillin/oxacillin +/- gentamycin or tobraycin
2.) Vanco + gent/tobra

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3
Q

Enterococcus species endocarditis

A

3rd major cause; usually preceded by bacteremia

Most frequently found following gu procedures in older men and ob procedures in younger women.

Virulence factors: pili, surface proteins, proteases and hyaluronidases.

Usually resistant to penicillin and carbapenems

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4
Q

Rheumatic Heart Disease

A

Following Strep. pyogenes pharyngitis in genetically predisposed individuals (people who make antibodies to Meromysin (M) protein.

Presentation: Mitral stenosis following pharyngitis w/ rash is a definitive clinical indicator

Damage due to type 2 hypersensitivity

Risk: strep throat (prolonged/untreated); prior case of rheumatic fever; ages 5-15 years old.

Sx: Usually appear 2 to 4 weeks after strep infx; pain and swelling in large joints; fever; weakness; muscle aches; SOB; chest pain

Dx: blood tests; throat culture; echo; CXR; EKG

Rx: Penicillin G; Aspirin; Steroids; Rest

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5
Q

Myocarditis

A

Inflammation of the myocardium. Usually caused by a viral infx (Coxsackievirus B and Adenovirus(children).

Sx: Chest pain, heart failure, and abnormal heart rhythms possible.

Cause of sudden death in children

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6
Q

Coxsackievirus B

A

ssRNA + (group IV); nonsegmented; icosahedral; nonenveloped; picornavirus; enterovirus

Cause of Myocarditis and Pericarditis

Palm and sole rash

Also HFM disease

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7
Q

Pericarditis

A

Inflammation of the pericardium. Typically an acute infection. Usually caused by a viral infx ( Cox A&B; Echovirus, and influenza.

Higher incidence in summer months (enterovirus peaks)

Sx: chest pain associated w/ irritated layers of the pericardium rubbing against each other.

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8
Q

Rocky Mountain Spotted Fever

A

Causative agent: Rickettsia rickettsii (dermacantor wood or dog tick) –> intracellular

Sx: fever, headache, abdominal pain, vomiting, and muscle pain. A rash may develop (hands and soles)

Rx: Doxycyline

Endemic areas are Oklahoma and eastward.

Pathology: Tick bite (carried by dogs, rodents), infx and proliferation in endothelial cells –> inflammation of endothelial cells of small blood vessels –> maculopapular rash of palms and soles spreading to the trunk –> widespread vasculitis –> headache and CNS changes, renal damage –> death.

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9
Q

COPD

A

Imaging: Flat diaphragms, hyper-expanded lungs, barrel chest, radiolucent lungs

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10
Q

Diaphragm paralysis

A

Imaging: Inspiration and expiration films or fluoroscopic evaluation (sniff test)

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11
Q

Tracheal deviation

A

Most common cause is goiter.

If can’t confirm w/ physical exam –> CT/MRI

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12
Q

Lymph node enlargement

A

Usually not visible on CXR

DDX: metastatic disease; lymphoma; reactive lymph nodes from infx (TB); granluomatous disease (sarcoidosis)

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13
Q

Congestive Heart Failure

A
Early pulmonary edema is interstitial
Late pulmonary edema is alveolar
Pleural effusions are common
Cardiomegaily is often seen
Kerley's B lines or septal lines are strongly suggestive
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14
Q

Pneumothorax (PTX)

A

Air between parietal and visceral pleura.

Seen in 30-40% of patients w/ blunt chest trauma, usually associated w/ rib fx

May be spontaenous or iatrogenic.

Tension PTX can be life threatening –> air accumulates due to one way valve mechanisms, causing increased pressure w/ vena cava compression and impaired venous return.

CXR findings: Sharp line = visceral pleura. No lung markings lateral.

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15
Q

Pulmonary Embolus

A

Clot in Pulmonary Artery.

3rd most common cause of CV death

Difficult to dx

CXR: Hampton’s hump: wedge-shaped opacity corresponding to lung infact

Westermark’s sign: relative oligemia

CT: dark grey w/ contrast in pulmonary arteries.

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16
Q

Aortic Dissection

A

Most common aortic emergency requiring immediate surgery

Tear in intimal layer of vessel separates intima from media or adventitia, causing a false channel. Eventually can burst.

Sx: Severe pain w/ tearing or ripping quality.

Risk factors: -HTN, Marfans or Ehlers-Danlos, cocaine, pregnancy.

CXR: wide mediastinum, abnormal arch configuraiton. L>R pleural effusion.

CT: Tubular bisected appearance of aorta. Often spiraled.

Ascending: surgical emergency, descending = medical mangagement.

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17
Q

Ectopia cordis

A

A failure in lateral folding.

Heart outside the thoracic cavity.

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18
Q

Congenital umbilical hernia

A

A failure in lateral folding

A defect in the muscle and CT or the anterior abdominal wall resulting in the protrusion of intestine and greater omentum through the defect

Skin and superficial fascia cover protruding mass usually located above or below the umbilicus

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19
Q

Exstrophy of the bladder

A

A failure in lateral folding

Urinary bladder opens onto the body wall

Results in extrophic bladder, hemipenis, hemiscrotum

20
Q

Congenital diaphragmatic hernia

A

Epi: 1/2200 newborns

Due to to defective development or failure of the pleuroperitoneal membranes to fuse w/ other diaphragmatic components; as a result, there is a posterolateral defect in the diaphragm (vertebrocostal or lumborcostal trigone)

Polyhdramnios (excess amniotic fluid) may be present

Defect is usually unilateral and on the left side becasue left periocarioperitoneal canal is larger than the right and closes later.

Left lung is hypolastic and heart and mediastinum are displaced to the right

Death of newborns due to failure of lung to develope (hypoplastic lung)

21
Q

Eventration of diaphragm

A

Half of diaphragm has defective musculature and abdominal viscera balloon into the thoracic cavity. Defect results mainly from failure of muscular tissue to extend into the pleuroperitoneal membrane of the affected side.

22
Q

Congenital esophageal hiatal hernia

A

Herniation of stomach through esophageal hiatus.

Due to failure of the esophagous to elongate sufficiently as the neck and thorax develop.

Congenitally enlarged esophageal hiatus may be the predisposing factor to adult hiatal hernia.

23
Q

Retrosternal (parasternal) hernia

A

Gut herniation between sternum/ribs and diaphragm

Greater omentum or gut may be present in the pericardial cavity.

24
Q

Valvular Stenosis

A

Valve doesn’t open fully

Chamber upstream has to develop more pressure during systolic phase in order to achieve a given flow through the valve

Increases “pressure” work (afterload) –> hypertrophy

25
Q

Valvular insufficiency

A

Regurgitant blood flow represents an additional volume that must be ejected in order to get sufficient forward flow.

Increases “volume” work (Stroke volume) –> chamber dialation

26
Q

Aortic stenosis

A

Characteristic signs:

  • Significant pressure difference between LV and aorta.
  • Intraventricular pressure rises VERY HIGH during systole and aortic pressure is subnormal in systole.
  • Low pulse pressure
  • High ejection velocity of blood leads to systolic murmur.
  • Cardiac hypertrophy and LV mass –> left axis deviation

Primary physiologic consequence:
-High ventricular afterload.

*often aortic valve is BOTH stenotic and insufficient. In this case both systolic and diastolic murmurs will be heard

27
Q

Mitral stenosis

A

Characteristic signs:

  • Pressure difference of more than a few mmHG across the mitral valve during diastole.
  • Elevated LA pressure
  • Diastolic murmur
  • May induce hypertrophy of left atrial

Primary physiologic consequence: high LA and pulmonary capillary pressure–> pulmonary edema –> SOB

28
Q

Aortic insufficiency

A

Characteristics:

  • Aortic pressure falls faster/farther than normal during diastole
  • Low diastolic pressure
  • Large pulse pressure
  • Ventricular EDV and EDP are higher than normal
  • Diastolic murmur

Primary physiological consequences:
-Reduced EF, increased volume workload

*often aortic valve is BOTH stenotic and insufficient. In this case both systolic and diastolic murmurs will be heard

29
Q

Mitral Insufficiency

A

Characteristic signs:

  • LA pressure is abnormally high
  • Left ventricular EDV and EDP increase
  • systolic murmur

Primary physiological consequences:

  • pulmonary HTN (SOB etc.)
  • Prolapse is the most common form –> valve leaflets evert into the LA during systole.
30
Q

Paroxysmal supraventricular tachycardia (PSVT)

A

Supraventricular arrhythmias

A rapid, usually regular rhythm, originating from above the ventricles. PSVT begins and ends suddenly.

Atria abnormally excited and drive ventricles at rapid rate.

EKG: QRS normal (but frequent); P and T may be superimposed

Sx: Low BP and dizziness common

31
Q

Sinus Node Dysfunciton:

A

Supraventricular Arrthymia

A slow heart rhythm due to an abnormal SA node. i.e. Sinus Arrest

32
Q

First degree heart block

A

Supraventricular Arrthymia

Unusually slow conduction.

EKG: Abnormally long PR interval (>0.2 sec); otherwise normal

33
Q

Second degree heart block

A

Supraventricular Arrthymia

Some, but not all, atrial impulses transmit through AV node due to slower than normal conduciton.

EKG: Some, but not all P waves accompanied by QRS & T wave

34
Q

Third degree heart block

A

Supraventricular Arrthymia

No impulses are transmitted through AV node, pacemaker defaluts to His (usually, not always), atrial and ventricuar rates are independent.

EKG: P waves and QRS are totally dissociated in EKG (P waves all spaced evenly from themselves and QRS are as well). Ventricular rate likely slower than normal becasue of alternate pacemaker –> often slow enough to impair CO.

35
Q

Premature atrial contracitons (PACs)

A

Supraventricular Arrthymia

Early extra beats that orginate in the atria

36
Q

Accessory pathway tachycardias

A

Supraventricular Arrthymia

A rapid rhythm due to an extra abnormal pathway or connection between the atria and the ventricles. The impulses travel through the extra pathways (Short cuts) as well as the normal AV-HIS Purkinje system. This allows impulses to travel around the heart very quickly causing tachycardia.

EKG: “delta wave” slurred upstroke to the QRS complex (due to a certain part of the ventricle firing first.

37
Q

AV Nodal Reentrant Tachycardia (AVNRT)

A

Supraventricular Arrthymia

A rapid heartrate due to more than one pathway through the AV node.

A tachy; A fib; A flutter

38
Q

Atrial tachycardia

A

Supraventricular Arrthymia

A rapid heart rate originating in the atria

39
Q

Atrial fibrillation

A

Supraventricular Arrthymia

A very common irregular heart rhythm. Many impulses begin and spread through the atria, competing for a chance to travel through the AV node. The resulting rhythm is disorganized, rapid, and irregular. Because the impulses are traveling through the atria in a disorderly fashion, it results in loss of coordinated atrial contraciton.

EKG: No P waves. Ventricular rate irruglar.

Often asymptomatic in terms of CO

40
Q

Atrial flutter

A

Supraventricular Arrthymia

An atrial arrhythmia cause by one or more rapid circuits in the atrium. Atrial flutter is usually more organized and regular than A fib (but more dangerous)

41
Q

Bundle Branch Block (Hemiblocks)

A

Ventricular Arrthymia

Occur in either of branches in purkinje system of IV septum.

Often due to MI

EKG: Widening of QRS (

42
Q

Premature ventricular contracitons (PVCs)

A

Ventricular Arrthymia

Early extra beats beginning in the ventricles. PVCs are common and often asymptomatic.

Can be related to stress, too much caffeine or nicotine, or exercise. Some PVCs can be caused by heart disease or electrolyte imbalance.

Single PVCs are common. Frequent occurrence is concern for myocardial damage or perfusion problems.

43
Q

Ventricular Tachycardia (V-tach)

A

Ventricular Arrthymia

A rapid rhythm originating from the lower chambers of the heart. The rapid rate prevents adequate filling. Very serious, often preceds V fib.

Usually by a ventricular ectopic focus.

Different types of V-tac:

  • generally ventricular contraction is less synchronous.
  • rapid rate of QRS
  • widening of QRS
44
Q

Long QT Syndrome

A

Ventricular Arrthymia

QT is prolonged if it is > 1/2 of the R-R, or >450ms?

Delayed ventricular myocyte repol.

Prolonged refractory period extends the vulnerable period when extra stimuli can evoke tachycardia or fibrillation (i.e. torsades de pointes)

45
Q

Torsades de pointes

A

Ventricular Arrthymia

Very serious. Odd type of V tach in that QRS complexes cyclicaly vary in amplitude around the baseline and can deteriorate rapidly into V-fib.

46
Q

Ventricualr fibrillation

A

Ventricular Arrthymia

Erratic disorganized firing impulses from the ventricles.

Medical emergency that must be treated w/ CPR and defribrillation ASAP.

EKG: Can’t discern P-wave or QRS. Can’t determine rate or rhythm. No PR interval.