FINAL EXAM part 7 - Skin/GIT Flashcards
Immunological reaction is activated by
The Langerhans cells, part of the innate immune system (in the epidermis) able to recognize allergens or hapten.
Atopic Dermatitis/Atopy is
-an Hypersensitivity Type 1 reaction (involve IgE antibodies, mast cells releasing histamine)
Dermatitis Herpetiforms is
- an Immune Complex Deposition, maintly IgA
- related to Celiac’s disease
Psoriasis:
- 90% are of P. Vulgaris type.
- Female and male equal risk
- Extensive proliferation of keratinoytes (abnormal composition–> squamous keratinocytes attached by filaments and fast turnover)
Acne:
- Hyperseborrhea with pro-inflammatory lipids
- Inflammation (increase with sebum blocking the duct)
- Propionibacterium acnes grows (when excess sebum+duct blocked)
- Epithelial proliferation (block the duct)
Skin Cancer:
-3 majors types: Basal cell carcinoma–> responsible for the formation of new cells (most common in Canada), Squamous cells (keratinocytes) and the Melanoma (melanocytes)
Dermatophytoses:
-Fungal infection (Athlete’s Foot)
Warts
- Cause by HPV
- Epidermal hyperplasia
- Cytoplasmic vacuoles (koliocytosis)
Achalasia is
- reduced vagal tone of the lower esophageal sphincter (LES), causing things to have difficulty getting into the stomach.
- Cause dysphagia.
- Due to neuronal loss in the lower regions of the enteric plexus (lose inhibition), it is tonocally inactivated and the sphincter stay closed.
Enteric nervous system covers which regions?
- From the oesophagus to the large intestine
- Submucosal plexus and Myenteric plexus
Hiatus hernia:
- Is when the lower part of the stomach and initial part of the stomach moves up into the diaphragm –> form a little pouch/hernia.
- Most common cause of GastroEsophageal Reflux Disease (GERD)
Type of cells in the stomach:
Parietal cells (secrete HCL) Chief cells (make pepsinogen) ->pepsin Mucuous neck cells (secrete mucous to protect us)
3 basic strategies used to treat ulcers:
- Neutralize the acid with antacids
- Blocking histamine
- Blocking the acid pump
Helicobacter Pylori mechanisms to survive in the pH of the stomach and to damage the stomach which are:
- Secrete enzyme (Urease) neutralizing the gastric acid
- Had Flagella for rotation and to burrow through the mucous
- Secrete exotoxins and enzyme dissolving the mucous
- Adhere tot he cells in our stomach via proteins on the cell surface
- Had Type IV secretion system, an injection system to inject damaging compounds and proteins right into the host cell in the stomach.
The 3 major ways the Helico Pylori destroys the epithelium of the stomach:
- Had neutrophil-activating protein (HP-NAP) that triggers intensive inflammation and injuries
- The Cag protein will be injected directly in the cell to kil it
- The VacA, a cytotoxin that forms pores inside the cell and will trigger apoptosis
Vomiting:
- Vomiting center in the medulla (many receptor like 5HT3 receptor)
- CTZ (no BBB) close to the Vomiting center
- Just before the vomiting: Glottis closed, Esophagus and lower esophagus sphincter relax ,high intrathoracic presure and intraabdominal pressure, Strong contrations of abdo muscles, antiperistalsis.
- During vomiting, (NO REVERSE PERISTALSIS) relaxation of the stomach which will cause the esophageal sphincter to open. all muscles pushing.
Cells types in the liver:
- Hepatocytes (able to regenerate)
- Kupffer cells (macrophages, able to phagocytose)
- Stellate cells (synthetic cells that can be activated to make collagen creating scare tissue and fibrosis)
Xanthoma:
Cholesterol deposits on the skin (around the eyes, creases of the hands)
Steatosis:
Steatohepatitis:
lipid accumulation in the liver
Lipid accumulation in the liver with inflammation
Hepatitis A (HAV):
- Contamination food
- The virus crosses the intestinal barrier, get into the blood, to the liver, reproduces itself, new particles get into the stool and it is shed into the stool.
- Symptoms disappear after a few weeks once the antibodies are made.
Hepatitis B (HBV):
- Attaches to the receptors on the surface of the hepatocyte, reproduce itself, is transmitted through blood, serum, and wound exudate (high concentration)
- moderate concentration of HBV: in the semen, vaginal fluid and saliva.
- 35% symptomatic acute hepatitis; 65% have subclinical infection (recovery)–> 10% will develop chronic hepatitis
Hepatitis C (HCV):
- many subtype, most common in Canada, type 1
- Distinguishing feature of HCV: take different shapes and size to latches onto lipoprotein (help protect the HCV), becoming a lipoviroparticle.
- Lipoviroparticle binds to the cells by recognizing CD81 and scavenger receptor (SRB1) on the surface of the hepatocyte.
- It hijacks the hapatocytes synthesis of lipoproteins.
Hepatitis D (HDV):
-HDV NEEDS HBV’s surface envelope, will coats itself in the HBV surface antigen. Both will begin to reproduce themselves and released into the blood.
Hepatitis E (HEV):
- No chronic state, same as hepatitis A.
- Acute illness can progress to fulminant hepatitis in pregnant women and lead to death of the mother and fetus.
Gallstones pathogenesis:
- Chronic hemolysis (overload the ability of the enzyme in the liver to conjugate it –> increase unconjugated bilirubin)
- Excess of cholesterol secreted in the bile –> obesity
- Very rapid weight loss
Volvulus:
-Intestinal obstruction where there is a twisting of the intestine that can come free and twist on itself.
Intussusception:
-Intestinal obstruction where one part of the intestine is pulled into the next part.
Diverticulosis:
- Low fiber diet cause more pressure in the intestine and tends to push this out causing pouches.
- Can infect –> diverticulitis
Secretory diarrhea:
- Secreting much mor that you’re able to absorbe
- Due to excess input of electrolytes (NaCl) with the water following.
Osmotic diarrhea:
- Happen to people who are intolerant to lactose
- Bacteria grow on it more than normally would (due to lactose not absorbed–>no lactase) and will causes water to be retained due to osmosis.
Diarrhea consequences:
Hypovolemia
Loss of K
Acidosis (loss of alkali from intestines)
Malnutrition (chronic)
Cholera:
-Cause diarrhea due to Vibrio cholerae produce a toxin which inserts in cell membranes in the intestine , causing G-proteins to be trapped in “ON” configuration, yielding sustained 2e messenger production. (will cause the cells pump out sodium and chloride, and water follow)
Rotavirus:
- The virus will damaged the villi, causing malabsorption
- Will increase secretion and impairs absorption, cause cell lysis
- damage the epithelial lining , which is where lactase is made –> can be intolerant to lactose for weeks.
Norovirus:
- Principal virus causing food poisoning, has antigen drift component. (so never immune, due to his frequent change)
- 24-48h
- Villus destruction and lactose intolerance
Salmonella:
- Bacteria causing food poisoning.
- Alter the normal microbiome in your intestine. Able to cross the intestinal barrier.
- Causing inflammatory diarrhea
Staphlococci:
- Bacteria that is a normal constituents on humans that caused food poisonning.
- Human touching the food anf the bacteria will grow on the food and release toxin
- Pre-formed, heat stable enterotoxin (even if heat or cook, still releasing their toxins)
E. coli:
- Major subgroups
- Enterotoxigenic E. coli (ETEC) cause gastroenteritis
- It increase secretion by stimulate a receptor which increase the output of sodium and chloride along with water.
