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Nutrition 452 > Final Essay questions > Flashcards

Final Essay questions Flashcards

1
Q

How is insulin released from Beta cells?

A
  • Glucose enters via beta cell in the pancreas
  • Phosphorylation by glucokinase
  • Glycolysis and generation of ATP takes place
  • Increase in ATP inhibits ATP sensitive K channels causing depolarization of B-cell membrane
  • Increase Ca influx via voltage sensitive Ca channels
  • Stimulation of insulin exocytosis
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2
Q

What are the different mechanisms underlying insulin resistance?

A

Abnormal b-cell secretory product
Circulatory insulin antagonists
Target tissue defects

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3
Q

What are circulatory insulin antagonists?

A
  • Anti-insulin antibodies
  • Anti-insulin receptor antibodies
  • Increased and increased levels of counterregulatory hormones (GH, corisol, glucagon or catecholamines)
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4
Q

What is the most common mechanism for insulin resistance?

A

Decreased number of receptors on the cell

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5
Q

What are the possible abnormal b-cell secretory products?

A

Abnormal insulin molecule

Incomplete conversion of pro-insulin to insulin

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6
Q

What are the possible target tissue defects?

A

Insulin receptor defect
Decreased number of receptors on the cell
Post-receptor defects
Glucose transporter (GLUT-4) cannot fuse with membrane –> low glucose flow into the cell
GLUT-4 vesicle may fail to translocate to membrane

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7
Q

What are the acute complications in diabetes?

A

hyperglycemia
hypoglycemia
ketoacidosis

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8
Q

What are the chronic complications in diabetes?

A

macrovascular

microvascular

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9
Q

Macrovascular disease(s)

A

atherosclerosis

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10
Q

Microvascular disease(s)

A

angiopathies
retinopathies
neuropathies
nephropathies

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11
Q

Consequences of hyperglycemia?

A

blood glucose levels —> glucose in kidneys —> glucose in urine (glucosuria) —> h20 excretion — urine volume and frequency increases (polyuria) —> thirst and frequent dehydration (polydypsia)

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12
Q

Consequences of hypoglycemia?

A
  • caused by not using drugs correctly or exercising too long, skipping or delaying meals, or consuming alcohol without any food (inappropriate DM management)

May result in permanent brain damage

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13
Q

Consequences of ketoacidosis?

A

lipolysis —> FA in blood —> ketone formation —> disturbance of acid base balance in blood (blood pH falls below 7.3) –> ketones in blood –> ketones in kidney —> ketones in urine –> cations in urine (Na, K)

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14
Q

What is the primary cholesterol carrier in the blood?

A

LDL

-high concentrations are related to coronary problems

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15
Q

How is LDL cleared from the blood?

A

LDL clearance is dependent on LDL receptors of and therefore the # and the activity of these receptors

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16
Q

Regulation of LDL receptor/High blood cholesterol levels

A
  • lower synthesis of cholesterol within cell-inhibits HMG-CoA reductase
  • stimulates storage of cholesterol as esters-activates acyl-CoA: cholesterol acyltransferase (ACAT)
  • decreases synthesis of LDL protein receptors
  • decreases amount of mRNA encoding the receptor-less receptors
  • why cholesterol has no where to go but scum up the arteries
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17
Q

Cycle of LDL receptors and cholesterol uptake

A

LDL receptor is a glycoprotein - binds LDL and starts a cascade effect
–the region with the receptor is called a “coated pit” coated with a protein called clathrin

When LDL binds the receptor, the coated pit pinches in to form a coated vesicle

The clathrin comes off the uncoated vesicle

LDL is uncoupled from receptor by a pH change-ATP proton pump

Receptors pinch off and are recycled back to the membranes

Uncoated vesicle fuse with lysosome for degredation of LDL to cholesterol and amino acids

Without sufficient LDL receptors, LDL remains in the blood and contributes to foam cell production

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18
Q

What is the link between PUFAs and inflammation?

A

Eicosanoids – they are mediators and regulators of inflammation derived from 20-C fatty acids

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19
Q

What are eicosanoids and what are they made from?

A

hormone like compounds usually made from polyunsaturated fatty acids

usually made from arachidonic acid based on dietary background

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20
Q

What are the types of eicosanoids?

A

prostaglandins (PGs)
thromboxanes (TXs)
leukotrienes (TXs)
and other oxidized derivatives

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21
Q

what is prostacyclin?

A

prostaglandin made by the blood vessel walls that is a potent inhibitor of blood clotting

type of eicosanoid

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22
Q

What is thromboxane?

A

stimulant of blood clotting made in the blood from PUFA

type of eicosanoid

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23
Q

What is leukotriene?

A

an important mediator of many disease involving inflammatory or hypersensitivity reactions, such as asthma

derived from fatty acids

type of eicosanoid

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24
Q

What is arachadonic acid?

A

omega-6 fatty acid with 20 carbons and four carbon-carbon double bonds

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25
What is eicosapentaenoic acid (EPA) ?
omega 3 fatty acid with 20 carbons and five carbon-carbon double bonds Present in large amounts in fish oils and is also synthesized in the body from alpha-linolenic acid
26
What is Docosahexaenoic acid?
omega 3 fatty acid with 22 carbons and six carbon-carbon double bonds Present in large amounts in fish oils and is also synthesized in the body from alpha linolenic acid
27
Different families of eicosanoids?
omega 3 and omega 6 fatty acids
28
How eicosanoids modify CVD risk?
dietary manipulations -- through the production of selected prostanoids and leukotrienes
29
omega 6 PUFAs
Linolenic acid--> Gamma -linolenic acid ---> arachidonic acid (found in meat)---> omega 6 derived eicosanoids thromboxane A2, proaggregatory Leukotriene B4, promotes white blood cell adhesion
30
omega 3 PUFAs
Alpha linolenic acid --> eicosapentaenoic acid (fish oil) --> docosahexaenoic acid ---> omega 3 derived eicosaniods prostacyclin PGI3, antiaggregatory thromboxane A3, less active leukotriene B5
31
What are the major forms of IBD?
Crohns disease | Ulcerative colitis
32
What are the clinical features of IBD>
chronic episodes of relapse and remission with varying degrees of duration and severity ``` diarrhea fever weight loss anemia altered GI transit malabsorption increased risk of colorectal cancer ```
33
What are the long term characteristics of IBD?
Malnutrition - weight loss and emaciation & vitamin and mineral deficiencies Growth impairment - especially in early adolescence`
34
What are the characteristics of crohns disease?
May involve any part of the GI tract (from the mouth to anus) -50-60% involve distal ileum and the colon inflammation may skip areas (skip lesions) Transmural - all layers of the mucosa affected
35
Long term complications of crohns disease?
Most common- blockage of the intestine/stricture Ulcers fistulas (ulcers that extend completely through the intestinal wall) Malnutrition (inadequate intake, intestinal loss of proteins, poor absorption)
36
Characteristics of ulcerative colitis
Involves only the colon and always extends from the rectum Affected are is continuous Confined to the mucosa (narrowing is uncommon)
37
Long term complications of ulcerative colitis?
Bleeding from ulcers Rupture of the bowel Sever abdominal distension - toxic megacolon
38
What are the nutrient needs for IBD?
Energy needs are not increased - unless weight gain is needed Protein needs increased by 50% -during active stages of disease Supplemental vitamins and minerals - vit b12 malabsorption, iron, calcium...vitamin k, zinc and selenium losses due to diarrhea Fat absorption is unaffected by UC but may be affected by CD (can occur with massive inflammation
39
What is the hallmark of cancer?
Immortality combined with uncontrolled cell growth
40
What are the characteristics of cancerous cell division?
Can divide without appropriate external signals Do not exhibit contact inhibition Can divide without receiving the all clear signal Are immortal - there is no limit to the number of times that they divide They invade local tissues They spread or metastasize to other parts of the body
41
What are the steps of the cancer process?
Initiation promotion progression
42
Initiation step of cancer process?
The beginning of the cancer process | Damage of DNA within cells (from carcinogenic agent)
43
Promotion step of the cancer process?
Clonal expansion of the initiated cell (activation of oncogenes by promoter agent) Rapid cycling - leads to even more mutations
44
Progression step of the cancer process?
Uncontrolled growth and spread (metastasis) of cancer cells to other parts of the body
45
What is metastasis?
The spread of cancer to other tissues of the body Cancer cells break away from the primary site and enter the bloodstream or lymphatic system
46
What are the common sites of metastasis?
lungs, bones, liver, brain depends on type, stage and location of original cancer
47
What is the process of metastasis?
- cells grow as a benign tumor in the epithelium - cells break through the basal lamina - cells invade capillaries (1 in 1000 cells will survive to form metastases) - the cells adhere to blood vessel walls in liver - the cells escape from the blood vessel (extravastation) - the cells proliferate to form metastasis in liver
48
What are the qualities that make cells cancerous?
- Self sufficiency in growth signals - Insensitivity to anti growth signals - Tissue invasion & metastasis - Limitless replicative potential - Sustained angiogenesis - Evades apoptosis
49
What are the genes implicated in cancer development
DNA repair genes Tumor supressor genes Proto-Oncogenes
50
What are DNA repair genes?
A number of genes and gene products that are responsible for the repair of mutations in DNA - the code for proteins that correct errors in DNA - Mutations in these genes lead to failure of DNA repair - Ex. xeroderma pigmentosa - Lack of nucleotide excision repair = increased skin cancer
51
What are tumor suppressor genes?
Anti-oncogenes that normally suppresses cell division at the G1 to S phase - a defect in these genes may be inherited (retinoblastoma in infants) - produces proteins to suppress tumor formation - restrains cell growth and division - Loss of tumor suppressors lead to uncontrolled growth and division ex. P53 is associated with > 70% of carcinomas and acts as a brake on cell division
52
What is P53?
A tumor suppressor gene "the guardian of the genome" -mutated in 70% of all human tumors - codes for p53 protein - halts cell growth and division - Initiates DNA repair - Irreversible damage : initiation of apoptosis
53
What are Proto-oncogenes?
normal genes with normal function in cell growth (tightly regulated) that can be stimulated (activated by mutation) to cause uncontrolled cellular differentiation - called oncogenes once they've undergone mutation, translocation and or amplification ex. Rous sarcoma - avian virus that converts normal genes into cancer causing genes (src oncogene)
54
What is an oncogene?
A positive regulator of cell proliferation Arises from the mutation of protooncogenes damaged genes whose presence and or over activity stimulates the development of cancer -instructs cells to make proteins ---> increase cell growth and division
55
Normal growth control
In normal cells: Cell growth and division is controlled by growth factors Enzyme activation cascades Transcription factors Normal cell growth and proliferation
56
Hyperactive growth
In cancer cells: Abnormal version/quantities of growth control protein are made causes the growth control pathway to become hyperactive Gas pedal The more active the pathway: the faster cells grow and divide
57
What is Ras?
Codes for G protein involved in normal cell signaling Located on chromosome 12 Activated by a mutation at any of 3 codons (12, 13 or 61) Mutations lock Ras into an active proliferative state - increases the rate if GDP/GTP exchange or decrease GTPase activity - --hydrolysis of GTP is blocked in mutant ras - --transcription is activated Proto-oncogene turned that is most frequently mutated in human cancers - 97% in pancreatic cancers
58
How do nutrients impact cancer?
Dietary factors can Block or enhance endogenous synthesis of carcinogens -induce enzymes involved in activation/deactivation of exogenous carcinogens -enhance/ameliorate (improve) oxidative damage to DNA -support inhibit normal DNA synthesis and cell division -Influence endogenous hormone levels, inflammation or irritation
59
What is the CDC classification system of HIV?
based on immune function and clinical status classified with a number, reflective of CD4 count and a letter, reflective of clinical status 1 = CD4 >500 (>29%), 2 = 200-499, 3 = <200 A = asymptomatic/acute, B = symptomatic, C= AIDS indicator condition Provides prognostic information for providers where a patient fits along the continuum of illness and as to what conditions if any they may be at risk for
60
What are the stages of HIV disease?
Acute HIV infection Asymptomatic chronic HIV infection AIDS or advanced HIV
61
What are the features of the acute stage of HIV?
4-7 week period immediately after infection Viral replication is rapid; very infectious Majority will develop flu-like symptoms (lasting a few days to a month) Within days HIV hides out into sanctuary sites (lymph notes, central nervous system) and remains dormant Seroconversion will occur
62
What are the features of the asymptomatic chronic stage of HIV?
Lasts a few months to 10 years Few if any symptoms Subclinical changes
63
What are the features of the symptomatic stage of HIV
Symptoms appear and often include: fever, sweats, skin problems, fatigue, and other non-AIDS defining symptoms There is a decline in nutrient statues or body composition
64
What are the features of advanced HIV stage (AIDS)?
one or more well defined, life-threatening clinical condition clearly linked to HIV-induced immunosuppression Actual diagnosis of AIDs is made when the CD4 count falls below 200 or when an AIDS-defining condition is diagnosed Once a diagnosis of AIDS has been made, it remains with the patient even if the CD4 count returns to above 200 with ART
65
When is the diagnosis of AIDS made?
Actual diagnosis of AIDs is made when the CD4 count falls below 200 or when an AIDS-defining condition is diagnosed Once a diagnosis of AIDS has been made, it remains with the patient even if the CD4 count returns to above 200 with ART

Nutrition 452 (7 decks)

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