Diseases Quiz 1 Flashcards
Strep viridans subacute infectious endocarditis
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
Staph Aureus Acute Infectious Endocarditis
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
Enterococcus species endocarditis
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
Rheumatic Heart Disease
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
Myocarditis
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
Coxsackievirus B
ssRNA + (group IV); nonsegmented; icosahedral; nonenveloped; picornavirus; enterovirus
Cause of Myocarditis and Pericarditis
Palm and sole rash
Also HFM disease
Pericarditis
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.
Rocky Mountain Spotted Fever
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.
COPD
Imaging: Flat diaphragms, hyper-expanded lungs, barrel chest, radiolucent lungs
Diaphragm paralysis
Imaging: Inspiration and expiration films or fluoroscopic evaluation (sniff test)
Tracheal deviation
Most common cause is goiter.
If can’t confirm w/ physical exam –> CT/MRI
Lymph node enlargement
Usually not visible on CXR
DDX: metastatic disease; lymphoma; reactive lymph nodes from infx (TB); granluomatous disease (sarcoidosis)
Congestive Heart Failure
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
Pneumothorax (PTX)
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.
Pulmonary Embolus
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.
Aortic Dissection
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.
Ectopia cordis
A failure in lateral folding.
Heart outside the thoracic cavity.
Congenital umbilical hernia
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
Exstrophy of the bladder
A failure in lateral folding
Urinary bladder opens onto the body wall
Results in extrophic bladder, hemipenis, hemiscrotum
Congenital diaphragmatic hernia
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)
Eventration of diaphragm
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.
Congenital esophageal hiatal hernia
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.
Retrosternal (parasternal) hernia
Gut herniation between sternum/ribs and diaphragm
Greater omentum or gut may be present in the pericardial cavity.
Valvular Stenosis
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
Valvular insufficiency
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
Aortic stenosis
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
Mitral stenosis
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
Aortic insufficiency
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
Mitral Insufficiency
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.
Paroxysmal supraventricular tachycardia (PSVT)
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
Sinus Node Dysfunciton:
Supraventricular Arrthymia
A slow heart rhythm due to an abnormal SA node. i.e. Sinus Arrest
First degree heart block
Supraventricular Arrthymia
Unusually slow conduction.
EKG: Abnormally long PR interval (>0.2 sec); otherwise normal
Second degree heart block
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
Third degree heart block
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.
Premature atrial contracitons (PACs)
Supraventricular Arrthymia
Early extra beats that orginate in the atria
Accessory pathway tachycardias
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.
AV Nodal Reentrant Tachycardia (AVNRT)
Supraventricular Arrthymia
A rapid heartrate due to more than one pathway through the AV node.
A tachy; A fib; A flutter
Atrial tachycardia
Supraventricular Arrthymia
A rapid heart rate originating in the atria
Atrial fibrillation
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
Atrial flutter
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)
Bundle Branch Block (Hemiblocks)
Ventricular Arrthymia
Occur in either of branches in purkinje system of IV septum.
Often due to MI
EKG: Widening of QRS (
Premature ventricular contracitons (PVCs)
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.
Ventricular Tachycardia (V-tach)
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
Long QT Syndrome
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)
Torsades de pointes
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.
Ventricualr fibrillation
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.
