Congestive heart failure (CHF) is a condition when abnormality of cardiac function is responsible for inability of heart to pump blood at a rate to meet the demands by peripheral tissues.
1. A. Systolic dysfunction: it is the consequence of progressive deterioration of myocardial contractile function as occurs with ischemic injury, volume overload, tachyarrhythmias, myocarditis and cardiomyopathy.
B. Diastolic dysfunction: it is the inability of ventricles to relax sufficiently during diastole due to thickened ventricular wall improper ventricular filling as in left ventricular hypertrophy, sustained HTN, aortic stenosis, congenital HD, AV shunts and myocardial fibrosis.
2. A. Forward failure: diminished cardiac output insufficient amount of blood pumped to the body, occur with disease of the heart.
B. Backward failure: decrease cardiac output stasis of blood behind the heart (in the venous system).
There are 2 types of CHF:
Left sided heart failure: caused by:
Ischemic heart disease.
Valvular diseases except mitral stenosis.
Symptoms and signs:
Pulmonary oedema dyspnea and paroxysmal nocturnal dyspnea.
Increased sodium-water retention and vasoconstriction increases workload on the heart.
Right sided heart failure: caused by:
Left side failure.
Congenital heart diseases.
Valvular diseases except tricuspid stenosis.
Symptoms and signs:
Jugular venous distension
Chronic congestive splenomegaly.
Chronic hypoxic renal congestion.
(exertional dyspnea, orthopnea, chronic cough, hepatomegaly, neck vein
distention, peripheral edema)
Risks in Adults with CHD
Arrhythmias (atrial fibrillation, atrial reentrant tachycardia, ventricular
tachycardia, ventricular fibrillation)
SA node and AV node disease
Multifactoral (most common)
Single gene mutations (fig. above)
Environmental factors (alcohol, lithium)
Signs and Symptoms:
poor feeding, sweating with feeding, tachypnea, tachycardia, cool extremities, diminished pulses, mottling, hepatomegaly
Children (similar to adults):
exertional dyspnea, orthopnea, chronic cough, hepatomegaly, neck vein distention, peripheral edema.(fig top one)
Deficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine)
Deficiency of trace elements (zinc, molybdenum)
Fungal contamination of foodstuffs
High content of nitrites/nitrosamines
Betel nut chewing
Burning-hot beverages or food
Long-standing esophagitis and Barret’s metaplasia
Plummer-Vinson syndrome( esophageal webs, microcytic hypochromic anemia and atrophic gastritis)
TP53 tumor supressor gene mutation
Long-standing celiac disease
replacement of the normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells
Prolonged and recurrent gastroesophageal reflux causes inflammation and eventually ulceration of the squamous epithelial lining. Healing occurs by ingrowth of progenitor cells and re-epithelialization by metaplastic columnar epithelium, thought to be more resistant absorptive enterocytes are not observedUlcer and stricture can occur,
30- to 100-fold greater risk of developing esophageal adenocarcinoma, hence, periodic screening for high-grade dysplasia with esophageal biopsy is recommended, and surgery or photodynamic ablation may need to be done.
salmon-pink, velvety mucosa between the smooth, pale-pink esophageal squamous mucosa and the more lush light brown gastric mucosa
Tongues extending up from the gastroesophageal junction, as an irregular circumferential band displacing the squamocolumnar junction cephalad, or as isolated patches (islands) in the distal esophagus
Squamous epithelium is replaced by metaplastic columnar epithelium
recognition of dysplastic changes in the mucosa that may be precursors of cancer is important.
Communication between the intra-abdominal splanchnic circulation and the systemic venous circulation
portal hypertension induces the formation of collateral bypass channels wherever the portal and systemic systems communicate
Portal blood flow is thereby diverted through the stomach veins into the plexus of esophageal subepithelial and submucosal veins, thence into the azygos veins and the superior vena cava
often it is eroded and inflamed because of its exposed position, further weakening the tissue support of the dilated veins
Among persons with advanced cirrhosis of the liver, half the deaths result from rupture of a varix, either as a direct consequence of the hemorrhage or from the hepatic coma triggered by the hemorrhage
Bleeding from concomitant gastritis, peptic ulcer, or esophageal laceration accounts for most of the remainder.
hemorrhage subsides spontaneously in only 50% of cases; endoscopic injection of thrombotic agents (sclerotherapy) or balloon tamponade is often required.
When varices bleed, 20% to 30% of patients die during the first episode.
Among those who survive, rebleeding occurs in approximately 70% within 1 year
Longitudinal tears in the esophagus at the esophagogastric junction
chronic alcoholics after a bout of severe retching or vomiting, but they may also occur during acute illnesses with severe vomiting
a hiatal hernia is found in more than 75% of patients with Mallory-Weiss tears.
Many pts with Mallory-Weiss tear have no antecedent history of nausea, retching, abdominal pain, or vomiting
Infection of the defect may lead to an inflammatory ulcer or to mediastinitis.
Even with severe blood loss, supportive therapy with vasoconstrictive medications, transfusions, and sometimes balloon tamponade, is usually all that is required
Boerhaave syndrome: rupture with pneumomediastinum, subcutaneous emphysema and mediastinitis
Esophageal instrumentation is the most common cause
incomplete relaxation of the lower esophageal sphincter in response to swallowing. This produces functional obstruction of the esophagus, with consequent dilation of the more proximal esophagus
Manometric studies show three major abnormalities in achalasia:
(1) aperistalsis, (2) partial or incomplete relaxation of the lower esophageal sphincter with swallowing, and (3) increased resting tone of the lower esophageal sphincter
Defect of intrinsic inhibitory innervation of the lower esophageal sphincter and smooth muscle segment of the esophageal body.
caused by Trypanosoma cruzi, which causes destruction of the myenteric plexus of the esophagus, duodenum, colon, and ureter;
polio, and autonomic neuropathy in diabetes
The wall of the esophagus may be of normal thickness, thicker than normal because of hypertrophy of the muscularis, or markedly thinned by dilation
The myenteric ganglia are usually absent from the body of the esophagus
Inflammation in the location of the esophageal myenteric plexus is pathognomonic of the disease
stasis of food may produce mucosal inflammation and ulceration proximal
progressive dysphagia and inability to completely convey food to the stomach. Nocturnal regurgitation and aspiration of undigested food may occur,
hazard of developing esophageal squamous cell carcinoma.
(A) Click to view.
(B) Click to view.
(A) Reserve cells in the transformation zone are continuous with the basal cells of the ectocervix and may undergo columnar and squamous metaplasia. Photomicrographs at bottom depict (from left to right) quiescent subcolumnar reserve cells, reserve cells undergoing columnar differentiation, reserve cells undergoing squamous metaplasia and ectocervical squamous epithelium (right).
(B) Schematic of the development of the cervical transformation zone.
Sialolithiasis (Salivary duct stones)
Sialadenitis (Inflammation of Salivary glands)
Viral e.g. mumps parotitis
Bacterial especially in postep. or dehydrated patient, and associated with sialolithiasis
Autoimmune chronic sialadenitis
e.g. Sjogren syndrome in RA causing xerostomia and keratoconjunctivitis sicca with lacrimal gland involvement Together called Miculiz syndrome
Chronic granulomatous sialadenitis,
e.g. TB, sarcoidosis
Salivary gland tumor
Warthin tumor, aka papillary cystadenoma lymphomatosum
Adenocarcinoma, squamous cell carcinoma and mucoepidermoid carcinom are rare.
Aphthous ulcers( canker sores)
Superficial erosions, often covered with a gray-white exudate and having an erythematous rim
triggered by stress, fever, ingestion of certain foods, and activation of inflammatory bowel disease
an autoimmune basis is suspected
Virus persists in a dormant state within ganglia about the mouth (e.g., trigeminal ganglia)
caused by fever, sun or cold exposure, respiratory tract infection, trauma
cold sores or fever blisters
Oral Candidiasis, thrush, moniliasis(fungal infection)
Diabetes mellitus, anemia, antibiotic or glucocorticoid therapy, immunodeficiency, or debilitating illnesses such as disseminated cancer
fungi can be identified within these pseudomembranes as boxcar-like chains of tubular cells producing pseudohyphae from which bud ovoid yeast forms
AIDS and Kaposi Sarcoma .
Leukoplakia refers to a whitish, well-defined mucosal patch or plaque caused by epidermal thickening or hyperkeratosis,
On microscopic evaluation they vary from hyperkeratosis to mild to severe dysplasia bordering on carcinoma in situ,
tobacco, particularly pipe smoking and smokeless tobacco (pouches, snuff, chewing), chronic friction, as from ill-fitting dentures or jagged teeth; alcohol abuse; and irritant foods, HPV
Cancerous transformation rate is greatest with lip and tongue lesions and lowest with those on the floor of the mouth.
Hairy leukoplakia: found in pts with AIDS and is not premalignant
Erythroplakia refers to red, velvety, often granular, circumscribed areas
the malignant transformation rate is >50%
Leukoplakia with marked epithelial thickening and hyperkeratosis.
HAV does not cause chronic hepatitis or a carrier state.
Case fatalities from HAV occur at a very low rate, when patients have preexisting liver disease from other causes such as HBV or alcohol
Close personal contact with an infected individual during the period of fecal shedding, with fecal-oral contamination, accounts for most cases and explains the outbreaks in institutional settings such as schools and nurseries
Because HAV viremia is transient, blood-borne transmission of HAV occurs only rarelyThe virus itself does not seem to be toxic to hepatocytes, and hence the liver injury seems to result from T cell-mediated damage of infected hepatocytes.
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