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General Pathology > 33B. Autointoxication ✅ > Flashcards

33B. Autointoxication ✅ Flashcards

1
Q

Definition of autointoxication

A

Endogenic toxicosis = self-poisoning
Internal source is causing a poisoning

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2
Q

7 types of autointoxication

A
  1. Disorder of intermedier metabolism
  2. Retention autointoxication
  3. Hepatic autointoxication
  4. Putrid autointoxication
  5. Abnormal direction of metabolism
  6. Enterogenic autointoxication
  7. Resorption autointoxication
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3
Q

/1. Disorder of intermedier metabolism as type of autointoxication

A

The transformation of a substance at a certain step of the intermediate metabolism gets stuck

No pathological pathway !

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4
Q

Diabetic autointoxication. Ketosis

A
  • “diabetic toxins”: ketone bodies are accumulated with a non-treated diabetes mellitus type 1: acetoacetate, beta-hidroxi-butirate, acetone
  • prolonged fasting (keto-diet)
  • ketone bodies are produced in the mitochondria of the hepatocytes from acetyl-CoA
  • result: ketone toxicosis = ketosis
  • ketone bodies and unprocessed fatty acids are decreasing the blood pH: ketoacidosis (metabolic acidosis)
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5
Q

Diabetic autointoxication (ketosis). Symptoms

A
  • nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain
  • acetone-breath
  • dehydration - dry mouth, decreased skin turgor
  • tachycardia and low blood pressure
  • cerebral edema, which may cause headache, coma, loss of pupillary light reflex and progress to death
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6
Q
A

Pancreas fibrosis in dog
Diabetic autointoxification

  • pancreas isn’t smooth, looks granulated
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7
Q

/2. Retention autointoxication. Meaning. Examples

A

The end products of normal metabolism are not excreted

Uremia. Uricosis. Icterus

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8
Q

Retention autointoxication. Uremia. Definition

A

Retention of various solutes that would normally be excreted by the kidneys, mainly
creatine, creatinine, urea, urine acid (birds)

Also hyaluronic acid, guanidine, guanidinoacetate, oxalate, SDMA (symmetrical dimethylarginine)

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9
Q

Complications of uremia

A
  • vascular damage -> haemorrhages, edemas
  • electrolyte abnormalities
  • renal osteodystrophy
  • multiorgan failure
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10
Q

Symptoms (and pathological lesions) of uremia

A
  • commonly in cats: ulcers in the mouth (urea from blood gets excreted to mucous membranes; urea will be broken down by bacteria to ammonia, which will damage mucosal cells -> necrosis on mucosal surface
  • damage of stomach mucosa
  • uremia encephalopathy (dilated blood vessels, edema)
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11
Q

?

A

Uricosis in birds

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12
Q

?

A

Granulomas in uricosis
Uric acid crystals act as foreign body —> granulomas

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13
Q

?

A

Uricosis.
Uric acid crystals act as foreign body —> granulomas

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14
Q

/3. Hepatic autointoxication

A

Hepatic parenchyma damaged (infection/poisoning/mechanical effect) —> fibrosis or cirrhosis

Fibrosis is followed by connective tissue proliferation
Cirrhosis = necrosis + regeneration + connective tissue proliferation

Systemic consequences:
- bilirubin retention
- gastro-enterogen autointoxication. Ammonia toxicosis. Hepatoencelopathy

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15
Q

Liver detoxification pathways

A

Phase 1
- oxidation, reduction and hydrolysis
- cytochrome P450 enzymes or Mixed Function Oxidase (MFO)
- membrane, hepatocyte
- chemical toxins

Phase 2
- conjugation (cystein, glycin, sulfur) to enable water solubility
- bile excretion
- urine excretion

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16
Q

Toxic effect of bilirubin

A
  • bilirubin is toxic in most biological systems tested
  • several mechanism have been suggested for this toxic effect, including inhibition of enzyme systems and inhibition of cell regulatory reactions (protein/peptide phosphorylation)
  • serum level of unconjugated bilirubin exceeds the albumin binding capacity —> bilirubin diffuses into the CNS —> permanent neurological damage or death
  • bilirubin encephalopathy with kernicterus
  • bilirubin-induced neurologic dysfunction (BIND): hypotonia, hypertonia, opisthotonus, retrocollis
17
Q

BIND - ?

A

Bilirubin-induced neurologic dysfunction

18
Q

/4. Putrid autointoxication

A

hystolyses produces toxin protein derivates (neurin, muscarin, mydatoxin = ptomains. Gangrene (tissue level). Inflammation + gangrene —> ichorous inflammation
—> sapraemia

19
Q

2 major types of gangrenes

A

Dry gangrene and wet gangrene

20
Q

Dry gangrene

A

Dry gangrene (gangrena sicca)
- Form of coagulative necrosis
- Affected part is dry, shrunken and dark reddish-black (because of haemostasis).
- Drying out prevents putrefaction
- With time lesion will separate from the body — autoaputatio

21
Q

Histology of gangrena

A
  • shrunk cells
  • hyperchromativ necked (kariopycnosis)
  • cells are integral
  • lack of autolysis, heterolysis
22
Q

Wet gangrene

A
  • damaged tissue can’t dry out
  • tissue is infected by saprogenic/saprophytic bacteria (e.g. Clostridium perfrigens or Bacillus fusiforms)
  • toxic products formed by bacteria are absorbed, causing systemic manifestation of sepsis
  • the affected part is edematous, soft, putrid, rotten and dark
23
Q

/5. Abnormal metabolism

A

Porphyria — is a condition when during the production of haemoglobin instead of the normal protoporphyrin 3 isomer the useless and toxic isomer 1 is being produced

(example for abnormal metabolism)

24
Q

/6. Enterogenic autointoxication, enterotoxaemia

A

Bacterial toxins produced inside the intestines cause an intoxication

Toxins were not just swallowed, but produced inside of the guts!!!

25
Q

Examples of Enterogenic autointoxication, enterotoxaemia

A
  • acute bovine pulmonary emphysema and edema (ABPEE)
    L-tryptophan -> 3-methylindole
  • equine grass sickness (Clostridium botulinum?)
  • infectious necrotic enteritis of piglets and chickens: Clostridium perfrigens
  • rabbits: E.coli, Clostridium perfrigens, Clostridium spiroforme
26
Q

Toxic colon

A
  • the colon’s function is to prevent the absorption and facilitate the elimination of toxins with the feces
  • toxins in the feces: indol, skatol, phenol, methylmercaptan, urobilin, histidine, ammonia, putrescine, neurin, cadaverin, butyric acid, cholin, methylguanidine
  • constipation causes intestinal autointoxication/toxic colon
27
Q

/7. Resorption autointoxication

A

Rupture, perforation or arrodation of the stomach or intestines will release content to the peritoneum, toxic compounds will be absorbed to the blood stream

Digested food + enzymes + blood + profuse bacterial contamination

28
Q

Morphological complications of the autointoxication

A
  • main affected organs: liver, myocardium, kidney, brain
  • hydronic or vascuolar degeneration: histopathologically large cytoplasm: swelling, enlarged mitochondria
  • toxic hepatopathy
  • toxic myodegeneration
  • toxic nephropathy
  • toxic encelopathy
  • DIC (disseminated intravascular coagulopathy/microthrombosis) -> vasculitis
29
Q

What’s the connection to autointoxication?

A

Haemorrhages are common in case of toxic material going through the body. Mainly haemorrhages happen under serous surfaces and often in the heart (lots of blood + pressure)

30
Q

DIC

A

General Pathology (19 decks)

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