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PATH 300 (Xavier) > FINAL EXAM part 7 - Skin/GIT > Flashcards

FINAL EXAM part 7 - Skin/GIT Flashcards

1
Q

Immunological reaction is activated by

A

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

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2
Q

Atopic Dermatitis/Atopy is

A

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

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3
Q

Dermatitis Herpetiforms is

A
  • an Immune Complex Deposition, maintly IgA

- related to Celiac’s disease

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4
Q

Psoriasis:

A
  • 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)
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5
Q

Acne:

A
  • 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)
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6
Q

Skin Cancer:

A

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

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7
Q

Dermatophytoses:

A

-Fungal infection (Athlete’s Foot)

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8
Q

Warts

A
  • Cause by HPV
  • Epidermal hyperplasia
  • Cytoplasmic vacuoles (koliocytosis)
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9
Q

Achalasia is

A
  • 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.
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10
Q

Enteric nervous system covers which regions?

A
  • From the oesophagus to the large intestine

- Submucosal plexus and Myenteric plexus

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11
Q

Hiatus hernia:

A
  • 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)
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12
Q

Type of cells in the stomach:

A 
Parietal cells (secrete HCL)
Chief cells (make pepsinogen) ->pepsin
Mucuous neck cells (secrete mucous to protect us)
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13
Q

3 basic strategies used to treat ulcers:

A
  1. Neutralize the acid with antacids
  2. Blocking histamine
  3. Blocking the acid pump
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14
Q

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

A
  • 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.
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15
Q

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

A
  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
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16
Q

Vomiting:

A
  • 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.
17
Q

Cells types in the liver:

A
  • 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)
18
Q

Xanthoma:

A

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

19
Q

Steatosis:
Steatohepatitis:

A

lipid accumulation in the liver

Lipid accumulation in the liver with inflammation

20
Q

Hepatitis A (HAV):

A
  • 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.
21
Q

Hepatitis B (HBV):

A
  • 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
22
Q

Hepatitis C (HCV):

A
  • 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.
23
Q

Hepatitis D (HDV):

A

-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.

24
Q

Hepatitis E (HEV):

A
  • 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.

25
Q

Gallstones pathogenesis:

A
  • 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
26
Q

Volvulus:

A

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

27
Q

Intussusception:

A

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

28
Q

Diverticulosis:

A
  • Low fiber diet cause more pressure in the intestine and tends to push this out causing pouches.
  • Can infect –> diverticulitis
29
Q

Secretory diarrhea:

A
  • Secreting much mor that you’re able to absorbe

- Due to excess input of electrolytes (NaCl) with the water following.

30
Q

Osmotic diarrhea:

A
  • 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.
31
Q

Diarrhea consequences:

A

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

32
Q

Cholera:

A

-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)

33
Q

Rotavirus:

A
  • 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.
34
Q

Norovirus:

A
  • Principal virus causing food poisoning, has antigen drift component. (so never immune, due to his frequent change)
  • 24-48h
  • Villus destruction and lactose intolerance
35
Q

Salmonella:

A
  • Bacteria causing food poisoning.
  • Alter the normal microbiome in your intestine. Able to cross the intestinal barrier.
  • Causing inflammatory diarrhea
36
Q

Staphlococci:

A
  • 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)
37
Q

E. coli:

A
  • 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.

PATH 300 (Xavier) (34 decks)

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