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Chemistry year 2 > Week 7 > Flashcards

Week 7 Flashcards

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1
Q

What is glucose

A

-monosaccharide
-circulates in plasma
-primary source of energy for organisms
-stored as glycogen in liver and muscle

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2
Q

What is hypoglycemia

A

-decreased glucose levels

diagnosed based on Whipple Triad
-hunger, sweating, nausea, dizzy, nervous, shaking
-plasma glucose is <2.8 mmol/L
-need glucose or glucagon

-can happen due to B cell tumors (insulinoma- making lots of glucose)

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3
Q

Fasting plasma glucose

A

FPG- plasma concentration of glucose after no caloric intake for 8-16 hours

ref 4-6

ONE OF 4 TESTS DIAGNOSTIC FOR DIABETES

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4
Q

Hyperglycemia

A
  • increase in glucose levels
    -diabetes mellites
    -fasting glucose levels are above 7 mmol
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5
Q

glycogenesis

A

glucose to glycogen for storage (liver and muscle) - DECREASED GLUCOSE

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6
Q

glycolysis

A

conversion of glucose to hexoses like pyruvate or lactate - DECREASED GLUCOSE

embden-myerhof - produces ATP

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7
Q

Glycogenolysis

A

breakdown of glycogen to glucose to use as energy by liver - INCREASE glucose

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8
Q

gluconeogenesis

A

-formation of glucose from non carb sources like AA, fatty acids - INCREASE GLUCOSE

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9
Q

lipogenesis

A

-conversion of glucose to fatty acids stored as adipose - DECREASED GLUCOSE

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10
Q

Lipolysis

A

decomposition of fat INCREASED GLUCOSE

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11
Q

what regulatory hormones are involved with
pancreas
pituitary
adrenal
thyroid

A

pancreas- insulin, glucagon and somatostatin - EXOCRINE and EDOCRINE function

pituitary - ACTH, GH

adrenal - cortisol, epinephrine

thyroid-thyroxine

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12
Q

What is insulin

A
  • acts as key to encourage uptake of glucose into cell
    -made by B cells of Islets of Langerhans in Pancreas
    -hypoglycemic agent , ONLY one that decreases glucose level
    -increases glucose uptake
    -stimulated/secreted by B cells for uptake when glucose levels are high

-NOT released when levels are low

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13
Q

What does insulin promote and inhibit

A

Promotes glycogenolysis
glycolysis
lipogenesis
protein synthesis

Inhibits formation of glucose
-glycogenolysis
- gluconeogenesis
-lipolysis

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14
Q

What is glucagon

A

made by ALPHA cells of islets of langerhans and secreted in event of low glucose levels
-HYPERGLYCEMIC AGENT - promoting glycogenolysis & gluconeogenesis

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15
Q

What are other hormones that raise glucose

Thyroxine - T4

A

-from thyroid stimulated by TSH
-glycogenolysis, gluconeogenesis
-increases intestinal glucose absorption

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16
Q

What are other hormones that raise glucose

Adrenocorticotropic (ACTH)

A

produced by anterior pituitary when responding to corticotropin-releasing hormone from hypothalamus in events of low cortisol
-stimulates adrenal cortex to make cortisol

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17
Q

What are other hormones that raise glucose

cortisol

A

produced by adrenal cortex
-gluconeogenesis & glycogenolysis
-reduces glucose use and uptake by peripheral tissues such as muscle & fat

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18
Q

What are other hormones that raise glucose

growth hormone

A
  • from anterior pituitary
    -antagonizes insulin-stimulated glucose uptake

-inhibit insulin

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19
Q

What are other hormones that raise glucose

Somatostatin

A

δ cells: pancreatic Islets of Langerhans
inhibits insulin

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20
Q

What is epinephrine

A

adrenline

-made by adrenal medulla gland
-inhibits, promotes glycogenolysis & lipolysis
-releases glucose for fight or flight response

inhibits insulin

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21
Q

What is hypoglycemia and what are the two types

A

Post absorptive -Fast
post prandial -reactive

-when glucose is low for too long the brain cant function properly
can have shaking, dizzy, drowsy, confusion

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22
Q

What is post absorptive or fasting
hypoglycemia

A
  • cant maintain stable glucose levels in fasting state - 2NDRY to other diseases

-drug/alcohol induced
-organ failure
-low ACTH, CORT, THYROXINE
- insulinoma - beat islet cell tumors (release of excess insulin)
-neonatal - transient hyperinsulinism

genetic defects: e.g. G6PD deficiency: Glycogen Storage Disease: glycogenolysis impaired

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23
Q

What is postprandial -reactive hypoglycemia

A
  • can happen after a meal
    -excess release of insulin causing glucose to drop below normal fasting levels (FAST GLUCOSE METABOLISM)
    -not as serious as post absorptive
    -alimentary GI surgery when food passes the stomach and goes into the intestien undigested which triggers insulin secretion
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24
Q

What is the most common cause of hypoglycemia

A

over-administration of insulin to a patient with diabetes (insulin shock)

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25
Q

What is hyperglycemia

A

-increase of blood glucose
-used by cells for energy -glycolysis
-converted to glycogen in liver (glycogensis)
-converted to fat (lipogenesis) and stored

GLUCOSE LEVELS STABILIZE

-when there is low or no insulin or if you cant use insulin = DIABETES MELLITUS

glucose stays high

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26
Q

Diabetes mellitus
Group of metabolic diseases” classified into

A

Type 1 diabetes
Type 2 diabetes
Gestational (GDM)
Other Specific Types (secondary disease)

ALL PRODUCE MODERATE TO SEVERE HYPERGLYCEMIA

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27
Q

What sample tube do you need for glucose

A
  • red or gold but grey is preferred

anticoagulant: K oxalate & sodium fluoride inhibits glycolytic enzymes (preserve glucose): NaF = grey top

anticoagulant: heparin = green top, light green PST tube

glucose in whole blood is 11% lower than in plasma

process quickly
glucose rate of stability in the FIRST HOUR - 5-7% loss

fasting is collect only 8-10 hours after fast

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28
Q

How to Improve Stability of Glucose?
in serum

A
  • centrifuge asap
    -remove serum from red cells in 1 hours
    -use sst
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29
Q

How to Improve Stability of Glucose?
in plasma

A

-centrifuge
-remove plasma from cells asap
-use PFT tubes
-analyze in 1 hour

needs Sodium Fluoride inhibits glycolytic enzymes (grey top)
provides stability for up to 24 hrs at room temp.

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30
Q

What is the reference method for glucose analysis

A

hexokinase

  • measure ABs of NADH at 340nm
    -Abs NADH is proportional to [] of glucose
    -method can be used for serum, plasma, urine, CSF
    -preservatives and anticoags dont interfere
    -hemolysis and increased bili can cause a false decrease
31
Q

What if random sample in above 11 mmol

A

hyperglycemia is diagnostic of Diabetes Mellitus

32
Q

Oral Glucose Tolerance Test (OGTT

A

-ADA) does NOT recommend OGTT
-diagnosis of Type 1 & 2 diabetes is controversial as FPG and OGTT may identify different patients with diabetes
-Poor reproducibility
-looks at bodys response to measured dose of glucose
-GDM at 24-28 weeks pregnant

33
Q

how do you prep a pt for OGTT

A

-must be healthy
-unrestricted carb intake for 3 days before test
-stop medications that interfere with glucose
-dont exercise , eat, drink or smoke before or during test
-you can drink water
-fast for minimum of 10 hours no more than 16
-test is done in AM because of hormonal diurnal effect on glucose
-collect fasting blwrk first
ggt0 is start of drink , blood at 2 hours with grey top

34
Q

What effects OGTT

A

-age, weight
-length of fast
-time of day
-what form of glucose was ingested
-medications
-how stressed you were

poor reproducibility

35
Q

renal threshold

A

concentration of a substance in blood where the kidney tubules cant reabsorb the substance

-9.4 mmol/L

if the concentration stays high then it will flush out through urine because the kidneys cannot reabsorb

36
Q

How is glucose handled in kidneys?

A

-filtered through the glomerulus
-reabsorbed by tubules
-not normally found in urine

uses sodium glucose transporter proteins

37
Q

When is glucose detected in urine

A
  • when blood glucose exceeds renal threshold like in Diabetes mellitus

-renal diabetes when the glucose DOESNT EXCEED the threshold but the pt has a LOWERED threshold
NOT a type of diabetes mellitus

38
Q

What is renal diabetes

A

benign, aysmp condition
-glycosuria WITHOUT hyperglycemia
-not related to diet
-NORMAL ogtt
-threshold DECREASED due to primary tubular defect in how glucose is handled by the body
-cant fully reabsorb the glucose
-NOT mellitus
-NOT deficiency of pancreatic insulin

39
Q

What is urine dipstick

A

enzymatic
-semi quantitative (approx 6 mmol/L
-more sensitive than Clinitest
-only detects glucose

-uses glucose oxidase and peroxidase reaction to detect glucose in urine with a chromogenic product

urine dipsticks were used to monitor insulin but now blood glucose meters are used

40
Q

What is glycosuria

A

glucose in urine
-qualitative test with no exact [], quick , none invasive done with dipstick

41
Q

When can you get a false neg or false pos with dipstick test

A

false positives:
strong oxidants e.g. bleach, other peroxides

false negatives:
reductants e.g. ketones, ascorbic acid (Vitamin C), salicylate (aspirin)

42
Q

What is galactosemia

A
  • Congenital deficiency of enzyme galactose-1-phosphate uridyl transferase that metabolizes galactose
    -causes increased Galactose in plasma and urine
    -give positive Clinitest and negative dipstick
    -babies cant thrive on milk as it has lactose
    -can lead to mental probs and cataracts , jaundice, enlarged liver, kidney damage

-galactose must be removed from baby’s diet (all milk products)

Galactose comes from Lactose that is broken down into Galactose and Glucose

43
Q

Urinary Sugar: Qualitative Test: Clinites

A

-copper reduction test which gives orange colour

  • tablet form
    -detects urine glucose AND other urinary sugars
    used to screen newborns for inborn errors of metabolism e.g. galactosemia

-not used as much because galactosemia is screened via heel prick

44
Q

What do the two types of diabetes result from

A

primary cause: decreased insulin action because it is the only hormone that lowers glucose

  • type 1 when the pancreas fails to secrete insulin - insulinopenia

type 2 - when insulin cannot act on the tissues = insulin resistance
-associated with obesity and sedentary lifestyle

45
Q

What is TYPE 1 autoimmune decrease of insulin

A
  • cellular mediated destruction of pancreatic islet B cells
    -absolute deficiency of insulin resistance
    -islet cell autoantibodies (ICA), insulin autoantibodies (IAA)
    can be detected before onset
    -interaction of genetic predisposition & environment

exposure to certain viruses can trigger an immune response that can lead to the development of autoantibodies

46
Q

how does type 1 diabetes present itself

A

Polyuria - increases urine production which decreases blood volume stimulating thirst

Polydipsia - excessive thirst - drinking loads of water to compensate for water loss

Rapid weight loss - insulin deficiency causes caloric loss, catabolism of fat and muscle

polyphagia- increased food intake

47
Q

why do you have excessive urinination and thirst in type 1

A
  • the extra glucose needs to be dissolved in water so it can be excreted so your body needs more water

kidney will try to make the urine isotonic so more water is moving to be with the excess glucose = excess urine production

hyperglycemia would mean that you have more glucose in extracellular plasma

48
Q

Diabetic Ketoacidosis (DKA)

A

Type 1 can lead to DKA
-decreased glucose uptake and increased fat metabolism which produces ketones - ketonuria and ketonemia - BHB, ACET
-metabolic acidosis - low pH >7 and low bicard

fruity smell to breath
severe dehydration
electrolyte abnormalities

49
Q

how do you treat type 1

A

no cure
insulin injections
you need to have strict control over diet
-goal is to MAINTAIN FASTING LEVELS

-monitor yourself with a glucose meter and adjust insulin dose yourself
-lab monitoring - A1C and urinary albumin excretion

50
Q

How does Type 2 come to be

A

-insulin resistance (insulin is produced; but body not responding)
-more subtle
-genetic factor
-Diabetic ketoacidosis uncommon

-prevent by exercising regulars

51
Q

What are the risk factors in type 2

A

> 40
-obesity, high BMI
-family history
-ethnicity
-GD
PCOS

usually middle aged

52
Q

Glucose Transport Molecule & Insulin Resistance

A

Glucose transporter: GLUT4

insulin-regulated glucose transporter found primarily in adipose found primarily in adipose tissues & striated muscle (skeletal and cardiac)

many drugs are being developed to enhance transport and bypass insulin receptor to activate GLUT4

53
Q

how to treat type 2

A
  • modify lifestyle - weight loss
    -oral hypoglycemic agent -
    Metformin Lowers glucose production in the liver
    – Improves body sensitivity to insulin (so insulin is used more effectively)

Sulfonylureas (tolbutamide, glipizide, glyburide): increase endogenous insulin release

Alpha Glucosidase Inhibitors:
– Injectables which slow digestion and lower sugar levels

most type 2 will need insulin eventually because as the disease progresses insulin will drop and they will be deficient /resistant to insulin

54
Q

What is GDM

A

-glucose intolerance in pregnancy
-risk to both mom and baby
-causes big babies or babies born with hypoglycemia (baby in mom exposed to high glucose so when its born it wont have that anymore)
-mom can have preclampsia

55
Q

Diabetes associated with secondary conditions:

A

pancreatitis
cystic fibrosis
islet cell dysfunction
genetic issues with B cell function or insulin action

56
Q

What are the complications with diabetes

A

can damage BV causing macro/micro vascular damage (fatty streak =stroke, occluded = leg amputation)
-retinopathy - blindness
-nephropathy - kidney failure

57
Q

What are some Macrovascular disease complications that arise from diabetes

A
  • affects large vessels
    -accelerated atherosclerosis - fatty plaques

Cardiovascular disease= stroke MI- leading cause of death in type 1 and 2

Peripheral vascular disease
-poor circulation in extremities
-foot gangrene

58
Q

What are some Microvascular disease complications that arise from diabetes

A

-affects small BVs
-mostly in type 1
-hyperglycemic probs

Retinopathy
-new bvs will burst because they are so fragile bleeding into the vitreous causing acute vision loss

Nephropathy/renal failure
-declining filtration rate
-thickening of glomerlulous BM
-increased excretion of urine protein = proteinuria
pt will need transplant

Neuropathy
-affects bv that supply nerves leads to neuropathy or loss of feeling
-gangrene can do undetected

59
Q

how does the lab help with diagnosing diabetes

A
  1. tests to diagnose Diabetes
  2. tests that monitor treatment for Diabetes
  3. tests that are indicators of diabetic complications
60
Q

blood tests for diabetes diagnosis

A

if you meet any ONE of these its a problem

Fasting plasma glucose ≥ 7.0 mmol/L (W7P1)

HbA1c ≥ 6.5 % (this lecture)

2- hr plasma glucose ≥ 11.1 mmol/L during an OGTT (W7P1)

Symptoms of hyperglycemia and random plasma glucose ≥ 11.1 mmol/L (W7P1)

61
Q

Other Blood Tests: not diagnostic for diabetes that you can do

A

Serum Na+
due to polyuria (urine loss)
Increased Na+ = shift of water from intracellular compartment to plasma (dilution of Na in plasma) = Decreased Na+

Serum K+ ↑ to compensate for acidosis:
-Low pH = H+ ions go into red cells and K+ ions leave red cells and go into plasma (hyperkalemia)
-kidney: H+ ions excreted in urine and K+ ions retained

Blood gases: pH ↓ , bicarbonate ↓ = metabolic acidosis
bicarbonate used up in buffering acidic ketones

Serum osmolality ↑: increased (due to↑ serum glucose

62
Q

Urine Tests
for diabetes that can be done but shouldnt be used for diagnosis

A

Dipstick Positive for urine glucose (glycosuria) when plasma levels above renal threshold of 9.4 mmol/L

Increased urine specific gravity (relative density) & Increased urine osmolality
-due to presence of glucose in urine
-results in excessive amounts of water and salt (electrolytes) being lost through urination = polyuria
-Difference btw Diabetes Insipidus, this is decreased

Positive urine ketones (urinalysis dipstick test): Type 1
acetone, acetoacetate, beta-hydroxybutyrate

63
Q

What tests are used to monitor diabetes

A

HBA1C - glycosylated hem
-glucose control over last 2-3 months since RBC have life span of 120 days
-increased if pt is not watching diet

fructosamine - interacts with albumin forms glycated albumin which is fructoamine not done as often because serum protein turnover rate is 2-3 weeks

renal function tests - to detect nephropathy
-albuminuria indicates diabetic kidney disease
-urea and creatinine are also increased

lipid profile - LIP2R increased means high rate of cardiovascular disease

64
Q

What is Glycosylated Hemoglobin / HbA1c

A

glucose covalently bound to amino of hem
-forms a ketoamine
-found in RBC of diabetic and non
-diabetes have a higher rate of glycation - ketoamine formation
-rate of glycation is directly proportional to the plasma glucose concentration

-used to assess long term glycemic control and pts developing condition , testing recommended 2x a year

65
Q

how is Hba1c measured

A

EDTA whole blood
-no centrifugation because we have to preserve hgb from hemolysis
-lysed RBCs are needed to test for hgb

Test for difference in charge
at specific pH glycosylated Hgb and non-glycosylated Hgb have different charges
–Ex. Cation-Exchange Chromatography: Glycosylated Hgb is less positively charged at neutral pH compared to Hgb A
-electrophoresis
-isoelectric focusing
-HPLC

Testing for structural diffs
Immunoassay: Antibodies are directed toward amino groups at the end terminal
–Both glycosylated Hgb and non-glycosylated Hgb are both measured

Affinity Chromatography: Glycosylated Hgb is separately eluted out based on chemical structure
** Preferred method bc it isn’t affected by other forms of Hgb

66
Q

What are some interferences when measuring HBA1C

A

Presence of abnormal Hb F, Hb S, Hb C
Cross-reactivity with some methods causing either falsely ↑ or ↓ results
Immunoassay doesn’t measure glycosylated Hgb F (ex. Thalassemia patients)
therefore, Glycosylated Hgb levels are FALSELY DECREASE

Hemolytic diseases or hemoglobinopathies
Decreased life span of RBC - falsely ↓ results
-Premature RBC death (decreased lifespan)
– Therefore, less time for Hgb to become glycosylated. Results are FALSELY DECREASED
– Fructosamine Test is an alternative (tests for proteins instead)

no standardized testing or reference method

67
Q

Diabetes Insipidus

A

NOT a form of diabetes mellitis
-pt has normal blood glucose not a disease of pancreas or insulin

ENDOCRINE DISORDER - HORMONE DEFECT- lots of urine
-cant concentrate urine - so urine is pale and dilute urine

68
Q

Diabetes Insipidus occurs due to

A

-Lack of pituitary Arginine Vasopressin Hormone (AVP) OR kidney fails to respond to AVP

-avp is found in hypothal and stored/secreted by posterior pit
-released due to increased plasma osmolality (low fluid in extra cellular fluid)
-body will respond by being thirsty but more fluid dilutes solutes
-avp will be released will act on collecting ducts of kidney to reabsorb more water which will dilute solutes in plasma reducing urine output but more concentrated

negative feedback system

ADH=AVP

69
Q

There are two types of AVP deff

A
  1. related to CNS disease
    trauma or damage to hypothalamus or pituitary results in failure to secrete
    neurogenic Diabetes Insipidus
  2. related to renal disease
    kidney doesn’t respond to normal levels secreted
    nephrogenic Diabetes insipidus
70
Q

What does Diabetes Insipidus present like

A

severe polyuria because the kidneys cant retain water since there is low/no AVP production
-children bedwet

Polydipsia - thirst , pt compensates by drinking alot of water

dehydration causes hypernatremia
-na levels are more concentrated in plasma due to water loss so high sodium can be fatal

71
Q

Diabetes Insipidus: Laboratory Investigation

A

Hypotonic polyuria – Hallmark for Diabetes Inspidus

Blood Tests
-serum osmolality ↑ >295 mmol/kg (due to increase in sodium)
-sodium ↑ (hypernatremia) >145 mmol/L
-serum AVP ↓ or ↑ (depends on Type of DI)
-vasopressin test not available in routine labs

Urine Tests
-osmolality ↓ < 300 mmol/kg = hypotonic urine*
relative density/specific gravity ↓ <1.005 (urine dipstick test)
-this is in contrast to Diabetes Mellitus (this is increase in specific gravity due to glucose)

Osmolality = 2 x sodium + glucose + urea

72
Q

Diabetes Insipidus : Water Deprivation Test

A

-Patient is deprived of water
-Patient should be releasing AVP to reabsorb water and urine should be very concentrated and less urine output

-measuring urine & serum osmolality
-hold water for 8 hours
-serial blood samples for serum osmo
-serial urine for urine osmo

if pt is healthy the kidney able to reabsrob water and output will be decreased
-any urine excreted will be concentrated with high osmo

if pt has Diabetes insp
-tubules fail to reabsorb water
-urine output increased
-urine is dilute with low osmo

73
Q

Urine/Serum Osmolality Ratio

A

urine osmolality mmol/kg/
serum osmolality mmol/kg

low Ratio in DI due to:
1). Urine osmolality is very low due to urine being dilute
2). Serum osmolality is very high due to concentrated sodium levels

74
Q

Treatment
of DI

A

IV FLUIDS to replace water
-DDVAP -desmopressin
synthetic AVP good for neurogenic DI since AVP isnt produced

aVP ↓
renal reabsorption of water ↓
urine volume ↑
urine osmolality ↓
plasma osmolality ↑

water deprivation: urine/serum osmolality ratio < 1

Chemistry year 2 (12 decks)

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