Path 2 - Alimentary 6

sihirlifil's version from 2016-11-21 11:27

Diarrhea Lab

Mechanisms of Diarrhea

Question Answer
What are the 4 basic mechanisms of diarrhea?Hypermotility
↑ permeability
Explain hypermotility's role in diarrheaNot really sure if 1° mechanism, bc usually absorption is quite rapid in normal circumstances. However, if there is already an intestinal dz, hypermotility would make it worse
Explain "↑ in permeability"'s mechanism in diarrheaNormally, some fluid will go from the gut wall to the lumen, but absorption of fluids in the intestine is more than the transmucosal leakage. If the transmucosal leakage exceeds the absorption, you can get diarrhea
What are the influencing factors (czs) which contribute to an ↑ in permeability of the mucosa?PORE SIZE/MUCOSAL INTEGRITY
(1) ↑ capillary hydrostatic pressure (portal hypertension, right heart failure, plasma volume expansion)
(2) Mucosal damage by viruses & bacteria
What does the liver usually end up looking like in portal hypertension (how does portal hypertension relate to diarrhea?) & what results are there?(Portal hypertension → ↑ capillary hydrostatic pressure → ↑ permeability)
Cz nodule hyperplasia w/ lots of fibrosis → then ↑ hypertension more → also liver isnt making enough proteins which ↓ oncotic pressure → ↑ hydrostatic pressure more
How does congestive heart dz relate to diarrhea?Pump not working well → things back up → ↑ push of fluids across intestinal wall into lumen → low grade diarrhea
↑ Permeability → what are 2 examples of things which can cz an osmotic pull to cz diarrhea(Luminal contents of the gut can osmotically “pull” fluids across the mucosal epithelium into the gut lumen)
2 examples are undigested food & ↑ bulk in the intestinal lumen (ie: you ate more food, you have more shit in there)
↑ Permeability → explain how lymph drainage can effect this, name specific condition related to thisImpaired lymphatic drainage → fluids not transported away from gut. Lymphangiectasis (pathological dilation of lymph vessels) is a condition which can happen when severe inflammation of the lamina propria damages or blocks the lymph vessels → leads to edema, infiltration of large #s of inflammatory cells
What is Johne’s Dz? (What czs it? how can you identify? what does it cz? Tx?)Czd by mycoplasma paratuberculosis. You will see tons of acid-fast bacteria on the Histopath. The body can't fight this pathogen well-but tries-& sends TONS of macrophages to the scene. Unfortunately, these macrophages just add to the problem by building up & getting in the way to cz malabsorption/occlusion of lymphatic vessels & the mucosa is thickened. Not Tx, must cull
Explain the hypersecretion mechanism of diarrhea (what is happening? what part is doing the secreting? ex?)It is ACTIVE secretion of electrolytes & water across the intestinal epithelium into the gut lumen. The loss of electrolytes/fluids is not czd by ↑ permeability, defective absorption or osmosis. Active secretion by the crypts. Ex’s incld cholera & "travelers diarrhea"(aka e coli)
Mechanism → malabsorption. How does maldigestion relate to this & what is the 1° situation?Not digested enough where body can absorb it (then czs osmotic pull to cz diarrhea), usually a pancreatic dz prob (↓ enzyme secretion)
Mechanism → malabsorption. How does motility relate to this?Intestinal stasis can cz malabsorption
Mechanism → malabsorption. What mucosal defect can affect this?Mucosal transport abnormalities can cz malabsorption
Mechanism → malabsorption. How does reduced lymphatic drainage (related: Lymphangiectasis, congenital or acquired) cz malabsorption?Infiltrate of inflammatory cells, neoplastic cells into lamina propria or lymphatics will block up the system

Selected Dzs Causing Mucosal Damage

Question Answer
What are the 3 viruses which replicate in the enterocytes → damage/kill enterocytes → ↓ absorption which leads to diarrhea?(1) Rotavirus
(2) Coronaviral enteritis
(3) Parvoviral enteritis
Where on the villi does Coronavirus attack?Basically the whole length of the stick-out portion of the villi (you are ALL king if you wear the crown, not just partly)
Where on the villi does Rotavirus attack?Basically distal half (top half portion)
Where on the villi does parvovirus attack?In the CRYPTS not really on the vili
Who does Rotavirus usually affect & when?(Can be humans & all domestic animals, but ex's:) Usually calves (1st week of life) & piglets (up to 7wk of age). either way, happens around the time where the animals are being weaned (enteral dz happens BC of reduction of milk-associated anti-Rotaviral antibodies)
Pathophysiology of Rotaviral enteritis (group A) (what happens, which leads to what?)Necrosis of enterocytes covering the upper ½ of the intestinal villi – loss of absorptive epithelium. Leads to malabsorption/maldigestion, secretion of Cl-(water then follows), there is also ↑ peristalsis bc virus activates the enteric nervous system. Also blockage of Na/glucose transport system (ROTAte 180* (which is half) & then immediately quickly spew out all the Cl, H20 & glucose)
What are the 3 animals he emphasized that got Coronaviral enteritis? Any special names for them?(1) Pigs - TGE (transmissible gastroenteritis)
(2) Calves (calf scours)
(3) Dogs
Once the virus stops its infxn/is dead, how long does it take the intestines to recover from their mucosal damage?Usually in just a few days (unless parvo bc that kills the regenerative cells of the crypts)
TGE is what, affects who, has what affect on the intestines?Transmissible gastroenteritis in pigs, CORONA VIRUS & czs short, stumpy villi (& diarrhea, obv). (Crown on a pig ass)
Parvoviral enteritis affects who? Has what affects?Cats (panleukopenia) & dogs (parvo). Bloody diarrhea! Affects crypts which means hard for intestine to regenerate. ALSO can cz peyers patch necrosis (they also have a ↑ metabolic rate so are desirable to the parvovirus)
What are the 2 types of damage a bacteria can cz to the mucosa?(1) Direct damage by invading
(2) Indirect damage by toxins
(often both happen)
What are the 2 bacteria mentioned to cz mucosal dzs?Salmonellosis, Clostridial enteritis (e coli doesnt really go INTO the mucosa, just stays on top of it)
Salmonellosis → is it zoonotic? G+ or G-? Does it cz direct or indirect damage? (Explain the damage process)YES zoonotic, also has nosocomial potential (can get in a hospital). Gram negative (salmon are-shaped not + shaped) & are enteroINVASIVE. They can invade cells directly through the epithelium OR through the M-cells (cells that are in peyers patches, transport things in to try to fight them). (Salmon can swim through the dam, or around the dam)
Describe the peracute (fastest), acute & chronic effects of Salmonella on the intestinePERACUTE = Petechial hemorrhages
ACUTE = Catarrhal (inflammation of a mucous membrane) enteritis w/ diphtheritic membrane (A false membrane formed on mucous surfaces). FIBRINOUS CHOLECYSTITIS (calves)
CHRONIC = Button ulcers (the salmon swimming patterns can be peracute, acute, or chronic)
Is the damage in Clostridial enteritis direct or indirect? → called what bc of this? Leads to __enteritisIndirect - Damage is czd by TOXINS so often called enterotoxemia
Czs hemorrhagic enteritis (Closed butt BLEEDING)
What is the agent which czs Clostridial enteritis? G+ or G-? How many types/groups & the groups are based on what?Clostridium perfringens, G+ ("t" in closetridium, looks like a plus)
There are 5 diff groups based on the TOXINS they produce (Type A, B, C, D & E)
How do you type the Clostridia perfringens?Typed A-E based on type of TOXIN it makes
What kind of effects do Clostridia have on the intestinal mucosa?Redness, hemorrhage, GAS CONGESTION
(ie: czs bubbles, makes gas which builds up in the mucosa, makes gas bc is anaerobic) (in the CLOSet bc farting too much)
What is ETEC? What dz's might it cz?Enterotoxigenic E. coli
This czs Neonatal E. coli in piglets, calves & lambs. Also Post-weaning E. coli diarrhea in pigs
Which E. coli czs neonatal E coli & post-weaning E coli?ETEC (enterotoxigenic E coli)
What is VTEC? What dz's might it cz?Verotoxigenic E. coli, czs edema dz of swine (VET treats edema swine, or VERA Wang walks in heels & then gets swollen piggies)
Edema dz of swine is czd by what?VTEC (verotoxigenic E coli) (a VET will treat edema in your piggies)
What is AEEC?Attaching-Effacing E. coli
What is EHEC?Enterohemorrhagic E. coli
What is the age of piglets affected by ETEC (neonatal E coli diarrhea)? What are the CS? What do you see on necropsy? How would you lab diagnose this?Age affected is usually a few hrs old to 1 week
CS are:
Watery diarrhea
Dehydration & vomiting
On necropsy youd see:
Watery feces
Flaccid intestines & clotted milk in the stomach
In the Laboratory youd:
Do culture to determine pilus & toxin type
What do the guts look like upon necropsy of neonatal E coli diarrhea (ETEC, enterotoxigenic E coli). Lesions? Gross appearance?Usually they are FILLED w/ FLUID, but you dont really see obvious lesions. Their toxins are producing an outflow of water & electrolytes into the lumen
What is the virulence factor of ETEC he mentioned & what does it allow?PILI! Bind to the epithelial surface of enterocytes & allow the bacteria to “hold on” & replicate to large numbers. (Also enterotoxins but he said we didn't need to go into detail)
On a Histopath, where do you expect to find the E coli in ETEC?Youd see them all stuck to the edge/border of the vili (stuck w/ their pili)...dont usually invade, just stick to the outside & produce toxins.
Explain the lesions the ETEC (enterotoxictoxigenic e coli) czs w/ their toxinsBiochemical, NOT mechanical....hijack machinery of cell, czs secretion of Cl- & then water follows → diarrhea