Diestion And Absorption Of Proteins Flashcards

1
Q

Are amino acids stored in the body?

A

NO

- quickly degraded if found in excess

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2
Q

What forms are most proteins absorbed as?

A

Tripeptides/dipeptides or AA’s

- use either facilitative diffusion or active transport in the intestinal brush border (similar to carbs)

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3
Q

Zymogen function

A

Pepsinogen = cleaved into pepsin spontaneously in acidic environments
- cleave peptides into smaller units in stomach

Tyrpsinogen = cleaved by enterokinase into trypsin

  • cleaves and activates other proteolytic enzymes such as: (chymotrypsin, elastase, carbooxypeptidases)
  • *also positive feedback on itself (cleaves activates itself and more of trypsinogen)
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4
Q

What controls pancreatic zymogen release?

A

The presence of CCK

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5
Q

Enteropeptidase

A

A serine protease that is found on the apical surface of brush border
- converts trypsinogen -> trypsin by removal of a hexapeptide From N-terminus

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6
Q

Gastric digestion of proteins

A

Begins in the stomach

  • HCl = cleaves/activates pepsin and also denatures proteins (makes it easier for pepsin to do its job)
  • pepsin = cleaves a few AAs off polypeptides
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7
Q

Celiac disease

A

Malabsorption disorder where an autoimmune reaction occurs in the presence of gluten
- triggers immune system to damage the brush border of the small intestine resulting in malabsorption of proteins and lipids, as well as some carbs

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8
Q

What are examples of pathology that can cause pancreatic secretion dysfunction

A

Chronic pancreatitis

Cystic fibrosis

Pancreatectomy

results in poor digestion and absorption of fats and proteins = steatorrhea and undigested proteins in feces

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9
Q

Aminopeptidase

A

Exopeptidase located on luminal surface of enterocytes

Cleaves N-terminal residue from oligopeptides

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10
Q

How are free amino acids absorbed?

A

Mostly by enterocytes at apical surface
- via sodium dependent secondary active transport from SLC proteins**

ONLY free AAs are released into the portal system via facilitated diffusion

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11
Q

How are Di and tri peptides absorbed

A

By proton-linked peptide transporters (pepT1)

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12
Q

What is the only amino acid transport system that is sodium-independent?

A

L system

  • branched and aromatic AAs
  • His/Met/Leu/Ile/Val/Phe/Tyr/Trp
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13
Q

Cystinuria

A

A disorder of the proximal tubule’s inability to reabsorbs cystine/arginine and lysine AAs as well as ornithine
- “COAL”

inability to reabsorption cysteine leads to accumulation and urinary tract stones

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14
Q

Hartnup disease

A

A mutation in B0 membrane transport protein system

  • cant reabsorption neutral amino acids in kidneys and intestines (especially Trp)
  • cant synthesize proper NAD(P) levels

Symptoms:

  • pellagra-like symptoms
  • inflamed skin
  • diarrhea
  • dementia
  • canker sores
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15
Q

What is the function of a proteasomes?

A

Ubiquitylation of damaged, short lived proteins or excess AAs
- uses ATP hydrolysis to unfold proteins

Cleaves ubiquinated proteins into AAs

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16
Q

Autophagy

A

The process of a cell to target long-lived, aggregated proteins and damaged organelles

  • encases it in a double membrane vesicle for elimination
  • also allows sometimes for reuse of basic molecular components for building blocks for cells
17
Q

How does nitrogen balance affect people?

A

(Nitrogen consumed - nitrogen excreted) = balance (+/-)

Positive balance = tissue growth

Negative balance = tissue damage

18
Q

Kwashiorkor vs marasmus

A

Kawashiorkor:

  • Protein depreciation and chronic malnutrition disorder
  • carbohydrate heavy/protein poor diets

Symptoms:

  • stunted growth
  • skin lesions
  • depigmented, course hair
  • bilateral pitting edema**
  • distended abdomen**
  • decreased serum albumin

Marasmus

  • overall calorie deprivation
  • deficiency in protien/carbs and calories

Symptoms:

  • extreme muscle wasting and cachexia
  • weakness
  • anemia
  • stunted growth
  • NO edema or distention of abdomen**
19
Q

Vitamin A effects

A

Works for vision, growth and differentiation

deficiency = night blindness and xerophthalamia

20
Q

Vitamin D effects

A

Calcium metabolism

*deficiency = rickets/osteomalacia *

21
Q

Vitamin K primary effect

A

Blood clotting

deficiency = spontaneous bleeding

22
Q

Vitamin E primary effect

A

Oxidative protection

deficiency causes hemolytic anemia

23
Q

Difference between fat soluble and water soluble vitamins

A

Fat soluble: (DEAK)

  • hydrophobic
  • stored in fat
  • slower onset
  • toxicity more common
  • steatorrhea causes malabsorption
  • AD are most common to be toxic in high doses

Water soluble (all B vitamins and C)

  • hydrophilic
  • excreted in urine
  • faster onset
  • uncommon for toxicity
  • NO deficiency relented to steatorrhea
24
Q

Deficency in niacin causes what?

A

Pellagra
- dermatitis, diarrhea and dementia symptoms

high doses of niacin inhibits lipolysis in adipose tissue

25
Q

What enzyme is auto analyzed for protein digestion?

A

Pepsinogen

- it auto cleaves itself in acidic conditions

26
Q

What does each micro mineral do as a function

A

Chromium -> insulin release

Copper -> enzyme cofactor

Fluorine -> bacteria resistance

Iron -> enzyme cofactor

Manganese -> enzyme cofactor

Zinc -> enzyme cofactor, compliment action, innate immunity

Iodine -> thyroid function

Selenium -> glutathione production

Potassium -> blood pressure

Cholride and sodium -> fluid balance and blood volume