FINAL EXAM part 7 - Skin/GIT

Question 1

Immunological reaction is activated by

Answer 1

The Langerhans cells, part of the innate immune system (in the epidermis) able to recognize allergens or hapten.

Question 2

Atopic Dermatitis/Atopy is

Answer 2

-an Hypersensitivity Type 1 reaction (involve IgE antibodies, mast cells releasing histamine)

Question 3

Dermatitis Herpetiforms is

Answer 3

• an Immune Complex Deposition, maintly IgA

- related to Celiac’s disease

Question 4

Psoriasis:

Answer 4

• 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)

Question 5

Acne:

Answer 5

• 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)

Question 6

Skin Cancer:

Answer 6

-3 majors types: Basal cell carcinoma–> responsible for the formation of new cells (most common in Canada), Squamous cells (keratinocytes) and the Melanoma (melanocytes)

Question 7

Dermatophytoses:

Answer 7

-Fungal infection (Athlete’s Foot)

Question 8

Warts

Answer 8

• Cause by HPV
• Epidermal hyperplasia
• Cytoplasmic vacuoles (koliocytosis)

Question 9

Achalasia is

Answer 9

• 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.

Question 10

Enteric nervous system covers which regions?

Answer 10

• From the oesophagus to the large intestine

- Submucosal plexus and Myenteric plexus

Question 11

Hiatus hernia:

Answer 11

• 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)

Question 12

Type of cells in the stomach:

Answer 12

Parietal cells (secrete HCL)
Chief cells (make pepsinogen) ->pepsin
Mucuous neck cells (secrete mucous to protect us)

Question 13

3 basic strategies used to treat ulcers:

Answer 13

1. Neutralize the acid with antacids
2. Blocking histamine
3. Blocking the acid pump

Question 14

Helicobacter Pylori mechanisms to survive in the pH of the stomach and to damage the stomach which are:

Answer 14

• 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.

Question 15

The 3 major ways the Helico Pylori destroys the epithelium of the stomach:

Answer 15

1. Had neutrophil-activating protein (HP-NAP) that triggers intensive inflammation and injuries
2. The Cag protein will be injected directly in the cell to kil it
3. The VacA, a cytotoxin that forms pores inside the cell and will trigger apoptosis

Question 16

Vomiting:

Answer 16

• 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.

Question 17

Cells types in the liver:

Answer 17

• 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)

Question 18

Xanthoma:

Answer 18

Cholesterol deposits on the skin (around the eyes, creases of the hands)

Question 19

Steatosis:
Steatohepatitis:

Answer 19

lipid accumulation in the liver

Lipid accumulation in the liver with inflammation

Question 20

Hepatitis A (HAV):

Answer 20

• 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.

Question 21

Hepatitis B (HBV):

Answer 21

• 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

Question 22

Hepatitis C (HCV):

Answer 22

• 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.

Question 23

Hepatitis D (HDV):

Answer 23

-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.

Question 24

Hepatitis E (HEV):

Answer 24

• 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.

Question 25

Gallstones pathogenesis:

Answer 25

- 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

Question 26

Volvulus:

Answer 26

-Intestinal obstruction where there is a twisting of the intestine that can come free and twist on itself.

Question 27

Intussusception:

Answer 27

-Intestinal obstruction where one part of the intestine is pulled into the next part.

Question 28

Diverticulosis:

Answer 28

- Low fiber diet cause more pressure in the intestine and tends to push this out causing pouches. - Can infect --> diverticulitis

Question 29

Secretory diarrhea:

Answer 29

- Secreting much mor that you're able to absorbe | - Due to excess input of electrolytes (NaCl) with the water following.

Question 30

Osmotic diarrhea:

Answer 30

- 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.

Question 31

Diarrhea consequences:

Answer 31

Hypovolemia Loss of K Acidosis (loss of alkali from intestines) Malnutrition (chronic)

Question 32

Cholera:

Answer 32

-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)

Question 33

Rotavirus:

Answer 33

- 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.

Question 34

Norovirus:

Answer 34

- Principal virus causing food poisoning, has antigen drift component. (so never immune, due to his frequent change) - 24-48h - Villus destruction and lactose intolerance

Question 35

Salmonella:

Answer 35

- Bacteria causing food poisoning. - Alter the normal microbiome in your intestine. Able to cross the intestinal barrier. - Causing inflammatory diarrhea

Question 36

Staphlococci:

Answer 36

- 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)

Question 37

E. coli:

Answer 37

- 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.