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Nutrition > TA Review Diseases and Minerals > Flashcards

TA Review Diseases and Minerals Flashcards

1
Q

coronary heart disease

A

-narrowing of arteries near the heart causing blockage

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2
Q

four stages of athersclerosis

A
  • healthy
  • fatty streak
  • atherosclerotic plaque
  • plaque rupture or erosion and thrombus formation
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3
Q

what is the underlying mech of the heart attack

A

-eruption of plaque

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4
Q

trans fats

A
  • forms during the hydrogenation of fats or naturally are in ruminant animals
  • increases LDL, potentially decreases HDL and increases CVD
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5
Q

saturated fats

A
  • solid at room temp
  • animal fats
  • increases LDL, which increases CVD risk
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6
Q

mono and polyunsaturated fats

A
  • these can decrease the risk and prevalence of heart disease
  • liquid at room temp
  • intake decreases LDL, which decreases CVD risk
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7
Q

omega 6 and 3

A

-omega 6 is more thrombotic and inflammatory and three is the opposite

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8
Q

omega 3

  • source
  • health benefit
A
  • foudn in both animals and veggies
  • marine fish oil is the best source
  • as you increase intak you drastically decrease your risk of sudden death
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9
Q

whole grains

  • CVD
  • mechanism
A
  • reduced risk for CVD

- mechanism: more fiber and phytonutrients; decreased risk of diabetes (controls glucose)

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10
Q

fiber and CHD

A
  • intake is inversely associated with CHD (for soluble and insoluble)
  • decreased total LDL; reduced glycemic and insulinemic response; food with fiber contains little saturated fats
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11
Q

physiological effects of soluble fiber

A

-decreases enterohepatic recirculation of bile acids by binding them and dragging them to excretion (this also ups cholesterol usage by making more bile acids which is good!); and decreases cholesterol absorption

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12
Q

phys effects of sugar

-specifically HFCS

A
  • cause weight gain

- HFCS is associated with weightgain, increased triglycerides, insulin resistance;

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13
Q

fructose metabolism

A

-bypasses glycolysis at a rate limiting step and goes straight to liver for hepatic metabolism

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14
Q

what are the two greates effects to weight loss

A

-increased physical activity and decreased sodium intake

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15
Q

pattern of a healthy diet

A

-more plant based food than animal food

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16
Q

foods in a healthy diet

A
  • whole grains
  • vegetables and fruit
  • low/nonfatdairy
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17
Q

nutrients of a healthy diet

A
  • nutrient dense
  • high in potassium
  • low in sodium
  • lower in SFA and trans fat
  • higher in PUFA and MUFA
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18
Q

liver synthesized materials

  • for local use:
  • for release into blood
  • for release into bile
A
  • local: amino acids, transaminase (liver enzymes), alkaline phosphatase
  • blood: urea, plasma proteins, lipoproteins
  • bile: bile acids, cholesterol, phospholipids
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19
Q

what does the liver store (vitmains, minerals, molecules)

A
  • glycogen
  • vitamin B12
  • fat soluble vitamins
  • iron/ferritin
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20
Q

liver fat metabolism

A
  • lipogenesis and lysis
  • FA esterification and oxidation
  • cholesterol, bile acid synthesis/degradation/esterification
  • lipoprotein formation
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21
Q

protein metabolism in the liver

A
  • produces: albumin, glycoproteins, transferrin, acute phase proteins, ceruloplasmin, clotting factors
  • urea formation
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22
Q

four stages of liver disease

A
  • inflammation
  • fibrosis
  • scarring
  • cirrhosis
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23
Q

liver fibrosis

A

-scarring and thickening of the liver

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24
Q

cirrhosis of the liver

A
  • chronic scarring

- irreversible and causes life threatening sequelae

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25
Q

liver disease leads to

A
  • hypoalbuminemia

- increase in protime/INR due to failure of hepatic synthetic function

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26
Q

causes of liver disease

A
  • infection
  • toxins
  • metabolic factors
  • immunological factors
  • altered circulation
  • biliary obstruction
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27
Q

hepatitis A spread

A

-fecal oral route

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28
Q

hep b spread

A
  • perinatal
  • blood
  • sexual transmission
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29
Q

hep c spread

-big diff between the other 2

A
  • blood transmission

- No preventative vaccine

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30
Q

alcoholic liver disease

  • cause
  • treatment
  • stages
A
  • alcohol is directly toxic to the liver
  • treatment is abstinence
  • stages: alcoholic steatosis, alcoholic hepatitic, alcoholic cirrhosis
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31
Q

alcoholic steatosis

  • cause
  • symptoms
  • treatment
A
  • may develop with transient alcohol use or chronic
  • fatty deposits in the liver
  • asymptomatic
  • reversible with abstinence
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32
Q

alcoholic hepatitis

  • cause
  • symptoms
A
  • develops after years of drinking

- fever, tender hepatomegaly

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33
Q

non-alcoholic fatty liver disease

  • stats
  • cause
  • hep manifestation of what
  • etiology
A
  • most common cause of liver disease in the US
  • caused by innapropriate management of lipids by the liver
  • fatty liver NOT caused by booze
  • hepatic manifestation of metabolic syndrome
  • possible insulin resistance fails to suppress the lipolysis of adipose (increased efflux of FFa from adipose which is sent to the liver)
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34
Q

non-alcoholic steatohepatitis

  • what is it
  • manifestations
A
  • extreme form of NAFLD
  • lipid accumulation and inflammation
  • due to second hit theory (possibly the presence of a virus)
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35
Q

risk factors for NAFLD

A
  • insulin resistence which causes: obesity, DM2, hyperlipidemia
  • female, rapid weight loss, parenteral nutrition, medications
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36
Q

progression of NAFLD to cirrhosis

A
  • NAFLD
  • NASH
  • cirrhosis
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37
Q

hemochromatosis

  • cause
  • what
  • patients have
  • manifestation
  • prevention to cirrhosis
A
  • iron overload syndrome
  • due to genetic mutation
  • iron deposition in liver leads to scarring and eventually cirrhosis
  • patients have high serum Fe/TIBC ratio
  • progression to cirrhosis can be prevented with phlebotomy, iron chelation therapy
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38
Q

wilsons disease

A
  • defect in biliary excretion of copper
  • leads to fatty infiltration, liver fibrosis and scarring, cirrhosis
  • concomitatn neuropsychiatricdisease
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39
Q

autoimmune hepatitis

  • manifestation
  • treatment
A
  • causes liver inflammation and eventual scarring

- treatment with steroids and immunosuppressive therapy

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40
Q

primary biliary cirrhosis

  • manifestation
  • treatment
A
  • leads to damage and destruction of bile ducts

- liver transplant

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41
Q

primary sclerosing cholangitis

  • leads to
  • associated with
  • treatment
  • seen in conjunction with
A
  • chronic cholestatic disease that leads to inflammation, fibrosis, and stricturing of medium and large bile ducts
  • associated with ulcerative colitis
  • liver transplant
  • seen in conjunction with ulceritis
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42
Q

cirrhosis

  • causes
  • leads to
A
  • nodule formation and liver fibrosis
  • causes: reduction in functional cell mass
  • leads to: hepatic encephalopathy, ascites, portal HTN, hepatorenal syndrome
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43
Q

portal HTN

A
  • hepatic fibrosis leads to increased resistance to blood flow through the liver so the blood backs up
  • leads to formation of varices
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44
Q

varices

  • cause
  • found in
  • what are they
  • clinical sig
A
  • caused by portal HTN
  • large dilated veins
  • found in esophagus, stomach, rectum
  • they bleed
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45
Q

ascites

A
  • accumulation of fluid in the peritonela space
  • due to elevated hydrostatic pressure from portal hypertension and from decreased oncotic pressure from hypoalbuminemia
  • treatment with paracentesis, diuretic treatment, dietary sodium restriction
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46
Q

hepatic encephalopathy

  • manifests as
  • etiology
A
  • decreased mental status
  • etiology: increased ammonia, false NT (LD amino acids greater than BCAA and cross the BBB and act like NTs to cause confusion)
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47
Q

treatment of hepatic encephalopathy

A
  • eliminate precipitating factors
  • supportive nutrition
  • lactulose or neomycin as medical treatments
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48
Q

energy requirements of patients with cirrhosis

A
  • vary
  • have the whole range of metabolism
  • normally the requirements are 120%-140% of REE
  • malnutrition is present in up to 80% of patients (more common in ALD)
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49
Q

malnutrition in LD patients is associated with increased risk of

A
  • variceal bleeding
  • refractory ascites
  • spontaneous bacterial peritonitis
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50
Q

causes of malnutrition in liver disease patients

A
  • metabolic abnormalities similar to sepsis or trauma

- an overnight fast for a liver disease patient is like a 72 hour fast for a normal person

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51
Q

protein restriction in liver encephalopathy

A
  • based on protein intolerance causes encephalopathy
  • not evidence based
  • common that patients with encephalopathy do not receive adequate protein
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52
Q

nutrition therapy with ACUTE encephalopathy

A
  • gradual increase in protein
  • small frequent meals and bedtime snack
  • vitmain and mineral supp
  • restrict Na/fluid if ascites. edema present
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53
Q

nutrition therapy with CHRONIC encephaolopathy

A
  • once encephalopathy resolves gradually increase protein to normal
  • use enteral supplements
  • encourage BCAA’s
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54
Q

nutrition therapy for liver disease patients without encephalopathy

A
  • do NOT restrict protein

- everything else is the same as acute encephalopathy

55
Q

liver disease and micronutrient status

A

-patients are at risk for def in all vitmains

56
Q

functions of the kidney

A
  • fluid balance
  • elimination of waste
  • acid base balance
  • formone production
57
Q

end stage chronic kidney disease causes

A
  • vitamin D not to be converted into the active form
  • decreased active form leads to increased PTH which leads to increased calcium via resorption from bone and secondary hyperthyroidism)
58
Q

definition of chronic kidney disease

A
  • damage to the kidney for greater than 3 months
  • structural or functional abnormalitis with OR without changes in GFR
  • manifests pathologically or with markers of kidney damage
59
Q

low GFR

A

-lower than 60mL/min/1.73 m2 for greater than 3 months

60
Q

diagnostic characteristics of the 5 stages of kidney disease

A
  • 1: kidney damage but normal kidney function
  • 2: kidney damage and mild loss of kidney function
  • 3: moderate loss of function
  • 4: severe loss of kidney function (symptoms begin)
  • 5: dialysis or kidney transplant required
61
Q

types of dialysis

A
  • hemodialysis: blood exchange

- peritoneal dialysis: solute infused into peritoneum and have exchange over peritoneum

62
Q

continual renal replacement therapy is used for

A

-acutely ill patients in the hospital

63
Q

effect of hemodialysis

A
  • cardio instability
  • nausea, vomiting
  • fatigue
  • protein losses of 6-8 grams per treatment
64
Q

effect of peritoneal dialysis

A
  • abdominal discomfort
  • glucose absorption
  • peritonitis
  • protein losses of 8 to 10 g per day
65
Q

causes of renal failure

A
  • metabolic disease, DM lupus
  • hypertension, damage to renal vessels
  • glomerulonephritis
  • obstructive disease, stones
66
Q

3 goals when treating kidney disease

A
  • delay progression
  • treat complications
  • renal replacement therapy
67
Q

nutritional related concerns of renal patients

A
  • malnutrition
  • sodium and fluid management
  • potassium regulation
  • phosphorus regulation
  • bone health
  • anemia of renal disease
  • lipid disorder
68
Q

causes of malnutrition in CKD patients

A
  • delayed gastric emptying
  • endocrine disorders of uremia (insulin resistance and hyperthyroidism)
  • unpalatable or inadequate diets
  • taste changes
  • inflammation, infection, sepsis
69
Q

biochemical measurements of patients with CKD

A
  • albumin (marker for mortality of hydration status)
  • urea (serum BUN measures nitrogen portion of urea)
  • creatinine (decreasing can mean poor muscle mass, high can indicate poor dialysis)
  • potassium
  • phosphate
70
Q

sodium and fluid retention of renal disease causes

A
  • edema
  • HTN
  • SOB
  • stress on the heart
71
Q

dry weight

-therapy

A
  • weight at which all or most excessfluid will have been removed
  • weight at which a patient is without hypoer or hypotension
  • therapy: diuretics, ultrafiltration, diet modifications
72
Q

hyperkalemia can be found in what patients and effects what

A
  • renal patients due to reduced excretion

- effects heart rhythms and pumping ability

73
Q

when does hyperphosphatemia develop?

A
  • in renal patients when their GFR falls below 25 ml/min
  • soft tissue calcification because it binds serum calcium
  • secondary hyperparathyroidism
74
Q

what may contribute to high PO4 intake

A

-products containing additives

75
Q

PO4 binders

  • used for
  • different binders
A
  • used to prevent hyperphosphatemia
  • Al based associated with osteomalacia, adynamic bonoe disease, myopathy, and dementia
  • Ca based binders asociate with hypercalcemia
  • binders without these metals are an important break through
76
Q

anemia of renal disease

  • why
  • type of anemia
  • treatment
A
  • EPO formation is impaired
  • normocytic normochromic anemia
  • recombinant humant EPO (epogen) and iron supp
77
Q

mineral are absorbed as

A

-ions with different redox states

78
Q

solubility affected by

A
  • pH

- binding to insoluble substances in the gut

79
Q

mineral transport

  • transport mediated
  • chelation
  • paracellular
A
  • transporter mediated: regulated and saturable
  • chelation: absorption as ligand
  • paracellular: gut permeability (not regulated or saturable)
80
Q

heme iron

  • absorption
  • found in
  • sources
A
  • 25% of intake is absorbed
  • in Hb and Mb
  • meat, fish, poultry
81
Q

non-heme iron

  • absorption
  • what is it
  • sources
  • difference between heme iron
A
  • 15%
  • iron not complexed to a heme protein
  • grains (fortified), nuts, veggies and fruit
  • absorbed differently than heme iron and have a different bioavailability (higher for non-heme) and have a different process that contributes to their bioavailability
82
Q

heme iron absorption mech

A
  • taken up by heme transporter (membrane protein)

- Fe dissociates from heme and stored as mucosal ferritin

83
Q

non-heme iron absorption mech

A
  • needs to be reduced from Fe3+ to Fe2+ by Dcytb so can become soluble
  • taken up via divalent cation/ metal transporter (DMT1)
  • also stored as mucosal ferritin
  • vitamin C helps keep iron in reduced form so that absorption is easier
84
Q

regulation of iron absorption

  • luminal absorption
  • iron release from intestine adn reticuloendothelial cell system
A
  • iron is sensed in the intestinal mucosa; regulation by Dcytb and DMT1
  • hepatic sensing of iron or other signals; hepcidin released if hepatic iron is adequate which regulates iron efflux into circulation from intestine, liver, spleen and lymph nodes
85
Q

enhancers of non-heme iron absorption

A
  • reducing agents: acids (vitamin c is a big one; helps turn Fe3+ into Fe2+)
  • ligands/chelators: binding maintains the reduced form and are found in meat, poultry, fish, mucin, sugars
86
Q

inhibitors of non-heme iron absorption

  • 3 examples
  • mechanism
A
  • polyphenols (tannic acid in tea and red wines, chlorogenic acid in coffee)
  • oxalate: grains, fruit, vegetables
  • phytates: legumes, grains, rice, vegetables
  • divalent minerals: calcium, zinc (this is a big one), manganese
  • these usually bind to iron in the oxidized state and inhibit it from being reduced (most of these are in a vegetarians diet)
87
Q

regulation of iron absorption

A
  • mucosal absorption by the enterocyte via the Dcytb and DMT1
  • export from enterocyte is regulated by hepcidin: control ferroportin expression by reducing its expression
88
Q 
function of hepcidin
-mechanism
A
  • regulates iron absorption
  • hepatic sensing of iron increases hepatic hepcidin (if you have adequate stores, you will produce more hepatic hepcidin)
  • hepcidin regulates release from enterocytes and macrophages
  • hepcidin is released from the liver and then goes to the SI adn to macrophages where it decreases release
89
Q

hepcidin regulates what protein?

A
  • ferroportin expression
  • ferroportin is on the basolateral surface of enterocytes
  • ferroportin is a channel protein that allows iron to get into circulation from the SI
  • there are some enzymes on the BL that reoxidze Fe2+ so it can be transferred to transferrin
  • hepcidin signals the cells to internalize transferroportin
90
Q

herceptin

A

-degrades ferroportin on basolateral membrane

91
Q

iron turnover

A
  • Hb, ferritin and hemosidering degradation

- only approximately 2 of the 24 mg needed comes from diet

92
Q

losses of iron in the body

A
  • Gi (blood, bile, mucosal cells
  • desquamation of skin
  • urine
  • blood loss
93
Q

iron deficiency

  • stats
  • population at risk
A
  • most common nutrient def world wide
  • infants/young children (stores gone by 4 to 6 months)
  • adolescents
  • menstruating females
  • pregnant women
  • malabsorption syndromes
  • intestinal parasites
  • vegetarians
  • athletes
  • chronic gastrointestinal or other losses
94
Q

iron deficiency

  • onset of symptoms
  • results in
A
  • symptoms may occur prior to anemia
  • anemia (glossitis, angular stomatitis(irritated corners of mouth), koilonychia (spoon shaped nails), red blood cell changes)
  • fatigue and lethargy
  • cold intolerance
  • impaired psychomotor development
  • imparied intellectual performance
  • impaired immunity
  • adverse pregnancy outcomes
  • increased risk of lead poisoning!!
95
Q

treatment of iron def

A
  • assess etiology
  • address dietary factors
  • increase iron in food
  • iron supplements, can take with low dose of vitamin c
  • parenteral if necessary
96
Q

excess intake of iron

  • UL
  • getting rid of it
A
  • 45 mg/day
  • based on average GI effects
  • hard to get rid of because no physiologic excretion pathway
  • common cause of acute accidental overdose in children
97
Q

hereditary hemochromatosis

-how to not treat

A
  • reducing dietary iron is not effective

- due to a mutation in hepcidin

98
Q

african/bantu overload

A
  • genetic predisposition to excess abosrption
  • only with high iron intake
  • iron containers used for cooking and beer brewing
99
Q

copper

  • source
  • function
A
  • source: liver shellfish, meats, whole grains, nuts, seeds and legumes
  • function: cofactor for multiple enzymes, key roles in nerve function, transport of iron out of the enterocyte
100
Q

copper absorption

  • where
  • in what form
  • transprters
A
  • by stomach and duodenum
  • in reduced state
  • transporters: Ctr and DMT1
101
Q

mechanism of zinc induced copper deficiency

A
  • zinc supplementation induces metallothionein
  • metallothionein binds zinc and copper
  • copper gets trapped in the enterocyte and excreted
102
Q

mechanism of copper def due to

  • absorption
  • transport
  • reduced intake
A
  • absorption: upper GI surgery such as gastrectomy and gastric bypass and malabsorption
  • trannsport: use of zinc supps, Menkes disesae (genetic tranport disorder), DMT1 cimpetition
  • reduced intake
103
Q

manifestations of copper def (most common)

  • neuro
  • hematologic
  • secondary iron def
A
  • neuro: similar to def in B12 (if you treat B12 and it doesnt get better then treat copper), myelopathy in spinal cord, peripheral neuropaty
  • hematologic: anemia can be normo, micro, macro; leukopenia
  • secondary iron def
104
Q

less common manifestations of copper def

A
  • osteoporosis

- cardiovascular (increased cholesterol, cardiomyopathy)

105
Q

zinc sources

A
  • animal foods
  • cereal grains
  • vegetable
  • supps
  • endogenous bile and pancreatic secretions
106
Q

zinc digestions and absorption

A
  • digested from proteins and nucleic acids
  • absorption by small intestine: carrier mediated (ZIP4 and DMT1), chelation by amino acids, paracellular diffusion
  • similar inhibitors and enhancers as non-heme iron
107
Q

risk factors for zinc def

A
  • acrodermatitis enteropathica (autosomal recessive defect of zinc transport)
  • malabsorption
  • chronic diarrhea
  • vegetarian diet
  • poor diet
  • alcoholism
  • possibly DM and chronic kidney disease
108
Q

zinc deficiency causes

A
  • growth retardation
  • skin lesions
  • alopecia
  • diarrhea
  • infection
  • hypogeusia
  • hypogonadism
  • mental slowing
109
Q

dental caries

A
  • tooth decay
  • problem with children
  • preventable if get fluoride at young age (generally)
110
Q

periodontal disease

A
  • gum disease, can lead to tooth loss
  • gingivitis or pyorrhea
  • progression: plaque bacteria infects gums (this is the instigator of the disease, made of strep and lactobacilus), gums recede, bacteria infects jaw bone, jaw bone recedes, tooth loss
111
Q

oral lesions

A

-usually seen in immune compromised patients

112
Q

what exacerbates any oral disease?

A

immune dysfunction

-the mouth is a good indicator of the bodies health because it has a high turnover rate

113
Q

osteoradionecrosis

-who does it happen to

A

-happens in immunocompromised patients who have radiation therapy in head and neck area

114
Q

ventilator associated pneumonia

-when?

A

-happens when ICU patients inhale bacteria

115
Q

Dental caries (aka tooth decay) progression

A
  • this is infectious!!
  • plaque bacteria adhere to enamel turns dietary sugars into acid, acid then irritates the gums and demineralizes tooth enamel, bacteria and acid enter area under enamel (dentin) and destroy the tooth
  • if we intervene before the last step then the enamel can be remineralized
116
Q

fluoride effect on teeth

A
  • produces a more stable crystal structure
  • promotes remineralization of enamel (makes it resistant to acid changes by changing it to fluoroapetite instead of hydroxyapetit)
  • suppresses cariogenic flora
117
Q

sources of fluoride

A
  • toothpaste, rinses, water

- greatest effect is topical and throughout life

118
Q

what is the problem with being dentally impaired?

A
  • affects desire and ability to eat
  • quality of diet declines
  • food choices affect oral tissue which effects food choices
  • if maintain one arch can maintain nutritional quality of diet (if you lose that arch then have 30% decline in quality of food choices)
119
Q

nutrition vs diet

A
  • nutrition: systemic effect on the body
  • diet: pattern of food intake (how you eat, no two people eat same exact, its very different than nutrition, diet LEADS to nutritional status
120
Q

dilantin hyperplasia

A

-dilantin causes overgrowth of gums so when person chews they bite down on the gum and not the tooth which cuases pain

121
Q

what is the primary risk of choking and what is the reason for these

A
  • dentures

- primary contributor to death by choking (covers upper palate and we lose taste sensitivity)

122
Q

under nutrition can lead to what in oral health

A
  • poor oral development and growth
  • slow healing
  • decreased resistance to oral infections
  • increased tooth loss
123
Q

over NUTRITION (supps) and oral health

A
  • vitamin D tox: leads to defects in teeth development (striations in enamel and arches)
  • vitamin A tox: leads to defective tissue regeneration
124
Q

how DIET effects teeth

A
  • these effects are local to the oral cavity
  • sodas cause demineralization
  • vitamin c tablets, acidic
  • xerostomia (from drugs)
  • eating disorders (bulimia)
125
Q

cariogenic foods

A
  • simple sugars
  • starch when in mouth for long period of time for amylase to break down into simple sugars
  • differ from person to person
  • NOT related to its carb content; -what matters is the way it is presented to the plaque, not amount
126
Q

stephan curve

A

-shows that the amount of sugar doesnt matter, it matters how it is presented to the bacteria on the teeth

127
Q

critical pH for demineralization

A

5.2 to 5.5

128
Q

factors in eating patter that increase caries risk the most

A
  • frequent CHO intake
  • frequent intake between meals**
  • slow dissolving foods
  • frequent sipping**
  • xerostomia
  • lack of fluoride
129
Q

eating factors that decrease risk of caries

A
  • consuming infrequently
  • consuming fast
  • liquid in mouth (fast removal)
  • oral hygiene
  • fluoride
130
Q

pregnancy and oral health

  • when do teeth start to develop
  • peridontal disease during preg is associated with
  • by what age should children see the dentis?
A
  • oral bacteria transmitted to child from mother
  • childrens teeth start developing during 3rd month of pregnancy
  • 20% of primary teeth are calcified before birth
  • age 1
131
Q

early childhood caries caused by

A
  • Long bottle contact, sipping!!
  • immature dentition
  • plaque filled mouth
  • low saliva
132
Q

teen caries caused by

A

-soda!

133
Q

adult and elder caries caused by

A
  • medications that cause xerostomia
  • smoking cessation
  • hard candies and breath lozenges

Nutrition (18 decks)

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