MALABSORPTION SYNDROMES

(Can cause diarrhea, steatorrhea, weight loss, weakness)

Celiac Sprue: Autoimmune-mediated intolerance to gliadin (wheat, rye, and barley), leading to steatorrhea. Associated with people of northern European descent. Finding includes antigliadin antibodies, blunting of villi, and lymphocytes in the lamina propria.

Decrease mucosal absorption that primarily affects jejunum. Serum levels of tissue transglutaminase are used for screening. Associated with dermatitis herpetiformis. Moderately increases risk of malignancy, most often T-cell lymphoma.

Tropical Sprue: probably infectious; responds to antibiotics. Similar to Celiac Sprue, but can affect entire small bowel.

Whipple’s disease: Infection with Tropheryma whippelii (gram positive); PAS-positive macrophages in intestinal lamina propria, mesenteric nodes. Arthralgias, cardiac and neurologic symptoms are common. Most often occurs in older man.

Disaccharidase deficiency: Most common is lactase deficiency →milk intolerance. Normal appearing villi. Osmotic diarrhea. Since lactase is located at tips of intestinal villi, self-limited lactase deficiency can occur following injury (viral diarrhea).

Pancreatic Insufficiency: Due to cystic fibrosis, obstructing cancer, and chronic pancreatitis. Causes malabsorption of fat and fat-soluble vitamins (A, D, E, and K).

A beta-lipoproteinemia: ↓ synthesis of apo B →inability to generated chylomicrones→↓ secretion of cholesterol, VLDL into bloodstream → fat accumulation in enterocytes. Presents in early childhood with malabsorption and neurologic manifestation.

ESOPHAGEAL PATHOLOGIES

Achalasia: Failure of relaxation of lower esophageal sphincter due to loss of myenteric plexus (Auerbach). High lower esophageal sphincter opening pressure and uncoordinated peristalsis lead to progressive dysphasia.

“Bird’s beak” on barium swallow. Dilated esophagus with an area of distal stenosis.

Associated with increase risk of carcinoma.

Secondary Achalasia may arise from Chagas’ disease.

Gastroesphageal reflux disease (GERD): Commonly presents as heartburn and regurgitation upon lying down. May also present with nocturnal cough and dyspnea.

Esophageal varices: Painless bleeding of submucosal veins in lower ⅓ of esophagus.

Mallory-Weiss syndrome: Painful mucosa laceration at the gastroesophageal junction due to severe vomiting. Leads to hematemesis. Usually found in alcoholics and bulimics.

Boerhaave syndrome: Transmural esophageal rupture due to violent retching. “Been-heaving syndrome”.

Esophageal strictures: Associated with lye ingestion and acid reflux.

Esophagitis: Associated with reflux, infection (HSV-1, CMV, Candida), or chemical ingestion.

Plummer-Vinson syndrome (United States)-Paterson-Brown Kelly syndrome (United Kingdom):

                                               Triad of:

                                               Dysphasia (due to esophageal web)

                                               Glossitis

                                               Iron deficiency anemia.

Barrett’s esophagus: Glandular metaplasia-replacement of nonkeratinized (stratified) squamous epithelium with intestinal (columnar) epithelium in the distal esophagus. Due to chronic acid reflux (GERD). May becomes adenocarcinoma, results from reflux.

Esophageal cancer: Progressive dysphagea (solid to liquids), weigh loss.

Risk factors: Alcohol/Achalasia

                     Barrett’s esophagus

                     Cigarettes

                     Diverticulitis (Zenker’s diverticulum)

                     Esophageal webs (Plummer-Vinson Syndrome)

                     Esophagitis

                     Familial

CARDIOVASCULAR REVIEW

Coronary artery anatomy

RAC: (Right Artery Coronary)

          1) Marginal artery—supplies right ventricle.

          2) PD (posterior descending/interventricular artery)—supplies posterior septum.

          In the majority of cases, the SA and AV nodes are supplied by RCA. The 80% of the time, the RAC supplies the inferior portion of the left ventricle via the PD artery, one 20%, the PD arises from CFX.

LCA: (Left Artery Coronary)

          1)  Left anterior descending artery (LAD)—supplies apex and anterior interventricular septum.

          2) Circumflex artery (CFX)—supplies posterior left ventricle.

Coronary artery occlusion most commonly occurs in the LAD.

Coronary arteries fill during diastole.

The most posterior part of the heart is the left atrium; enlargement can cause dysphagia, due to compression of the esophageal nerve, or hoarseness due to compression of the recurrent laryngeal nerve, a branch of the vagus.

Auscultation of the heart.

Aortic area: Systolic murmur: Aortic stenosis.

                                                 Flow murmur.

                                                 Aortic valve sclerosis.

Pulmonic area: Systolic ejection murmur:

                                                 Pulmonic stenosis.

                                                 Flow murmur (e.g. atrial septal defect).

Tricuspid area: Pansystolic murmur:

                                                 Tricuspid regurgitation.

                                                  Ventricular septal defect.

                         Diastolic murmur:

                                                  Tricuspid stenosis.

                                                  Atrial septal defect.

Mitral area: Systolic murmur:  Mitral regurgitation.

                   Diastolic murmur: Mitral stenosis.

Left sternal border: Systolic murmur:

                                                  Hypertrophic cardiomyopathy.

                                Diastolic murmur:

                                                  Aortic regurgitation.

                                                  Pulmonic regurgitation.

Cardiovascular physiology.

Cardiac output (CO) = stroke volume (SV) x heart rate (HR)

Fick principle:

CO =                 rate of O2 consumption

          Arterial O2 content – venous O2 content

MAP (mean arterial pressure)

TPR (total peripheral resistance)

MAP = CO x TPR

MAP = 2/3 diastolic pressure + 1/3 systolic pressure

Pulse pressure =systolic pressure – diastolic pressure

Pulse pressure is proportional to stroke volume.

SV = CO = EDV – ESV

          HR

During the exercise, CO increase initially as a result of an increase in SV. After prolonged exercise, CO increase as a result of an increase in HR.

If HR is too high, diastolic filling is incomplete and CO decrease, e.g. ventricular tachycardia.

Stroke volume is affected by contractility, afterload, and preload. When increase preload, decrease afterload, or increase the contractility, the stroke volume increase.

Contractility and SV increase with:

1)      Catecholamines (increase activity of Ca 2+ pump in sarcoplasmic reticulum).

2)      Increases intracellular calcium.

3)      Decrease extracellular sodium (decrease activity of Na+/Ca2+ exchanger).

4)      Digitalis (increase intracellular sodium, resulting in increase calcium).

Contractility and SV decrease with:

1)      β1 blockade.  

2)      Heart failure.

3)      Acidosis

4)      Hypoxia/Hypercapnia.

5)      Non-dihydropyridine Ca2+ channel blocker.

    

SV increases in anxiety, exercise, and pregnancy.

A failing heart has decrease SV.

Myocardial O2 demand is increases by:

1)      ↑ afterload

2)      ↑ contractility

3)      ↑ heart rate

4)      ↑ heart size

Preload = ventricular EDV.

Afterload = MAP and proportional to peripheral resistance.

Preload increases with exercise (slightly),↑ blood volume (overtransfusion), and excitement (sympathetics).

Preload pumps up the heart.

Force of contraction is proportional to initial length of cardiac muscle fiber (preload).

Ejection fraction (EF).

EF is an index of ventricular contractility; it is normally ≥ 55%.

EF = SV        = EDV – ESV  

       EDV              EDV

The resistance is directly proportional to viscosity, and inversely proportional to the radius of the 4^th power. This means that is the radius of a blood vessel doubles by vasodilatation, then the flow will increases 16 fold. On the other hand, is the radius of the vessel is reduce in half, by vasoconstriction, then the blood flow will be reduced16 fold.

The viscosity depends mostly on hematocrit.

Viscosity increase in:

1)      Polycythemia.

2)      Hyperproteinemic state.

3)      Hereditary Spherocytosis.

Cardiac cycle.

Phases—left ventricle:

1)      Isovolumetric contraction; period between mitral valve closure and aortic valve opening (highest O2 consumption).

2)      Systolic ejection: period between aortic valve opening and closing.

3)      Isovolumetric relaxation: period between aortic valve closing and mitral valve opening.

4)      Rapid filling: period just after mitral valve opening.

5)      Reduced filling: period just before mitral valve closure.