Cardio Flashcards

Question

An 80-y/o woman reports that her mother told her she had rheumatic fever as a child. Which valvular abnormalities might she have?

Answer 1

Mitral stenosis, aortic regurgitation, mitral valve prolapse, mitral regurgitation, tricuspid regurgitation

Answer 2

Severe hypotension and bradycardia Ace inhibitors, nitrates and peripheral alpha 1 selective adrenergic blockers- **vasodilation** and **reflexive tachy cardia**

Answer 3

An **A**bsence of either s*eptum primium or septum segundum during development* Findings: fixed S2, HF, pulmonary hypertension, Eisenmenger Syndrome [vs patent foramen ovale is failure of septum primium and septum segundum to fuse during develpemt]

Answer 4

Thiamine = B1 Primary function is the ***decarboxylation of the alpha keto acids*** for carbohydrate metabolism A deficiency could lead to: **BeriBeri** --\> peripheraly neuropathy, HF *wet or dry depending if there is cardiac involvement (wet obvi = cardiac involvement)* **Wernike-Korsakoff syndrome** **\*alcoholics** "In extreme cases, beriberi is associated with Wernicke-Korsakoff syndrome. Wernicke encephalopathy and Korsakoff syndrome are two forms of brain damage caused by thiamine deficiency. Wernicke encephalopathy damages regions of the brain called the thymus and hypothalamus. This condition can cause confusion, memory loss, loss of muscle coordination, and visual problems such as rapid eye movement and double vision. Korsakoff syndrome is the result of permanent damage to the region of the brain where memories form. This can cause loss of memory, the inability to form new memories, and hallucinations."

Answer 5

Marfan's: Auto dominant on Chrom 15, affecting fibrillin-1 gene and thus the elasticity --\> **CYSTIC _MEDIAL_ NECROSIS** that leads to issues such as aortic dissection, aneurysm MVP, aortic regurg.

Answer 6

Rhabdomyomas #1 cardiac tumor in children TS is an **autosomal dominant** syndrome characterized by _cutaneous angiofibromas_ (adenoma sebaceum), _seizures_ and _mental retardation_

Answer 7

Turner: XO **Bicuspid** aortic valve **PREductal** coartcation of aorta (aortic narrowing before the insertion of the ductus arteriosus)

Answer 8

FA is **spinocerebellar dedegration** marked by spinal ataxia could produce difficulty walking/gait ataxia auto RECEssive associated with- **hypertrophic cardiomyopathy** **[lot of other stuff]**

Answer 9

Could be due to aplical lung tumor, thrombic occlusion.. **_ONE SIDED_ arm, face and neck swelling** VS: ***Superior Vena Cava Syndrome*** - you get _BILATERAL_ arm, face and neck swelling

Answer 10

The **AV node** is located on the endocardial surface of the right atrium, near the insertion of the septal leafet of the tricuspid valve and the orfice of the coronary sinus **Ablation** could occur here to correct a fib that is non-responsive/intolerant to therapy

Answer 11

*Low molecular weight* **heparins** such as ***enoxaprin*** ***(NO warfarin; aspirin and clopidogrel have no effect on ACUTE VTE treatment)***

Answer 12

Acetylcholine, bradykinin or shear stress can cause an _increase in calcium_ --\> NO formation via **Arginine, NADPH and O2** --\> NO + citrulline --\> activation of **GC** and an **increase in cGMP via GTP** --\> activates **protein kinase C** --\> *_decrease in cytosolic calcium_* and relaxation of smooth muscle

Answer 13

In *_pacemaker cells_*, phase 0 depolarization is primarily due to **calcium influx** [also note, pacemaker cells do not have phase 1 and phase 2, and phase 4 is a slow depolarization, via I channels] VS in *_myocardiocytes and purkinje cells_*, phase 0 depolarization is due to **sodium influx**

Answer 14

3rd and 4th phary. pouch * Caused by*: **anterosuperior displacement of the infundibular septum** 1. **o**verriding aorta 2. **v**entricular septal defect **3. \*\*pulmonic infundibular stenosis \*\*** *_most important determinant for prognosis_* 4. **r**ight ventricular hypertrophy * boot shaped heart on CXR* "PROV" Pulmonary stenosis forces right to left flow across VSD --\> early cynatoic tet spells (*blue baby syndrome*) **relived by SQUATTING** -- increased systemic ventricular resistance, RED right to left shunt, improves cyanosis; a low SVR:PVR raion, allows the deoxy blood from the right ventricle to take the low resistance output to the system --\> acute hypoxemia/**tet spells**; the squatting increases the SVR thus, forces blood through the pulmonic circulation **Treatment is early surgical correction**

Answer 15

AAA --\> chronic transmural inflammation/_transmural_ inflammation --\> dedegration of elastin and collagen --\> loss of elastin, and abnormal collagen remoldeling/cross-linking --\> weakening and expansion of the aortic wall = aortic aneurysm Atherosclerosis: intima changes Aortic dissection: intimal tear with dissection of blood through media of the aortic wall Marfan - cystic medial necrosis (predisposing to aortic dissection and AAA), characterized by loss of smooth muscle, collagen and elastin --\> cystic mucoid spaces in the aortic _media_ _Syphillis heart disease -_ **vaso vasorum endarteritis**/tree barking

Answer 16

Key players: endothelial cells, vascular smooth muscle cells, leukocytes 1. Endethelial cell injury via chronic hemodynamic stress and hyperlipidemia 2. INC expression of surface vascular cell adhesion molecules (VCAMs) --\> 3. migration of monocytes adn T-lymphocytes into intima 4. infiltrating leukocytes and dysfunctional endothelium release cytokines and growth factors that promoate the migration and proliferation of smooth vascular muscle within the intima 5. SVM, then promote extracellular matrix deposition and the formation of the fibrous cap