exam 2 study guide

produces microcytic cells

what type of cells does iron deficiency anemia make?

dietary intake of iron below minimum requirement

chronic blood loss

impaired duodenal absorption of iron

severe liver disease

what are the causes of iron def. anemia?

iron def. anemia

very common and ranges from mild to severe

common in women of childbearing age with menstration and pregancy

frequently a sign of an underlying problem

rarely due to diet alone

d/t bleeding issues

fly people like to dance

stomatitis and glossitits

brittle hair

spoon hsaped nails

mentraul irreg.

poor wound healing

what are the s/s of iron def. anemia?

low rbc/hgb

low iron

low ferritin

rbc microcytic and hypochromic

positive occult stool

how do we dx iron def. anemia?

treat underlying cause

iron replacement therapy with food supplements

what are the tx for iron def. anemia?

pernicious anemia

dietary insufficiency of b12

low absprtion secondary to atrophy of gastric mucosa

autoimmune reaction

chronic gastric inflammation

gastrectomy

resection of ileum

macrocytic cells

vit b12 deficit cuases demyelination in the peripheral nerves

affects sensory fibers first, motor fibers second

effects may be irreversible

describe the realtionship of b12 and nerve cells ?

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glossitis

nausea, diarrhea

nursing, numbness, tingling, d/t demyelination of the nerve fibers in the periphery first

what are the s/s of pernicious anemia?

rbc low, macrocytic with few in the peripheral blood

bone marrow is hyperactive

serum b12 low

how do we dx pernicious anemia?

monthly im injections of vit b12

what is the treatment of pernicious anemia?

genetic condition

autsomal recessive disoder

causes change in the hemoglobin molecule

common in middle eastern or african ancestry

what are the causes of sickle cell anemia?

autosomal recessive trait

sickle cell trait Aa

sickle cell anemia aa

what kind of genetic trait is sickle cell anemia?

larger vessels occluded

cases infarctions throughout the body

extremely painful

obstruction can lead to infarction and areas of mecorsis, ischemia, pain

sickle cell shaed cells are often too large o pass through microcirculation and causes pain

NBS unstable and changes to sickle shape with hypoxemia

what is a sickle cell crisis?

sever pain d/t oschemia

hyperbilirubinemia

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splenomegaly

small fibrotic spleen

vascualr occultoin and infarctions

delay growth and development

what are some of the s/s of sickle cell anemia?

because the liver cant get rid of the bilirubin because of the amount of cells death and cant keep up causing yellowing of the skin.

why does hyperbilirubinemia occur with sickle cells anemia?

in the lungs

smaller blood vessels

cerebral infarction

where do vascualr occulations nad infarctions occur with sickle cell anemia?

impariment or failure of bone marrow

can affects all of the body

idopathic

myelotoxins

hep c

autoimmune disordes

geentic abnoramilties

what are the causes of aplastic anemia?

normocytic

manifestatiosn are a result of pancytopenia

low rbc

low platelet

low wbc

what are the s/s of aplastic anemia?

bone marrow biopsy may be needed

how do we dx aplastic anemia?

id the cause and remove the bone marrow suppressant

possible bone marrow transplant

failure to tx is life threatening

what is the tx for aplastic anemia?

hemphilia A

classic hemophilia

deficit or abnormaility of clotting factor 8

most common type of hemophilia

x linked recessive

describe the genetics of hemophilia A

.5% normal factor 8 activity

prolonged bleeding after minor tissue trauma

describe minor hemophilia

,1% normal factor 8 actiivty

spontaneous bleeding

most common type

describe severe hemophilia

hemoarthosis

epistaxis

hematuria

hematoma

bloody stools

prologned bleeding after surgery and vaccines

what are the s/s of hemphilia?

serum factor 8 is low

partial thromboplastin time is prolonged

coagulation time is prolonged

how do we dx hemophila?

factor 8 replacement

desmopressin which caues enodthelial vessels to released stored factor 8

how do we tx hemophilia?

disseminated intravascular coagulation

always indicates anthoer underlying disease

excessive bleeding and clotting

thromboplastin activates the clotting process throughout the body

depletion of platelets and clotting factors

pregnancy complications accounts for 50%

infection

carinomas

burns

crush injuries

what are the causes of DIC?

blleding at 3 or more unrelated sites

platelet count low

fibrinogen declinging

pt,ptt thrombin time elevated

how do we dx DIC?

find the cause

how do we tx DIC?

leukemia

neoplastic disorder of wbc

overproduciton of wbc

4 types acute vs chronic

lymphoid vs myeloid

acute leukemia

lots of imamature nonfunctional blast cells

multiply excessivly

sudden onset

onbious s/s

chronic leukemia

mare mature cells with reduced functon

multiply sloer

gradual onset

mild s/s

better prognosis

unknown

radiation

virus

chemical exposure

chromosomal abnormalities

what are the causes of leukemia ?

infection that does not respond to tx

excessive bleeding

what is the onset of leukemia marked by?

overp roduction of leukemic cells causes decreased production of normal cells

decreased functional wbc

decreased rbc

decreased platelents

weight loss, fatigue

CNS changes in leukemic cells infiltrate the brain

what are the s/s of leukemia?

perihperal blood smears that show immautre leukocytes and altered numbers of wbc

numbers of rbc and platelets decreased

bome marrow biospy for comfirmation

how do we dx leukemia?

chemo

all young children respond well to drugs

biological therapy to stimulate immune system

how do we tx leukemia?

lack of response by cells to insulin

deific of insulin secretion by beta cells in teh pancreas

what is DM caused by?

autimmune disorders that causes the desctuction of beta cells

acute onset

most common in children/ adolescents

what are the causes of type 1 diabetes?

resistance: pancrease resistant to glucose levels

body cells resistant to insulin

beta cells less reposnvie to plasma glucose level

onsidious onset

more often dx in adults

most common type of dm

body cells less responive to the d/t the high levels of glucose for a prolonged time

what are the causes of type 2 dm?

genetic and family history

what are the risk factors of type 1 dm?

obestiy

older adults

african american, hispanic, native amreican

family hx

hx gestational diabetes

metabolic syndrome

what are the risk factors for type 2 dm?

polyphasic

decreased movement of glucose into the cells elading to cellular starvation triggering hunger

hyperglycemia

blood glucose levels rise

glycosuria

excess glucose on the blood spills into the urine

polyuria

due to tincreased osmotic pressure, pulls lots of water with it

polydispa

hypovolemia nad hyperglycemia=cell dehyration leading to thirst

polyuria. polydipsia, polyphagia

glycosuria

nocturnal enuresis

fatigue

weight loss

progresive ketoaidosis/ketouria

metabilic ketoacidosis

what are the s/s of type1 dm?

may or may not notice the cardinal s/s

insidious onset of hyperglycemia, pt ay be asymptomatic

weight gain, increased abdominal girth.

what are the s/s of type 2 diabetes?

random bgl.200 with polyuria, polydypsia and wt loss or grain

serum fasting bgl.126

hgb a1c .6.5 % confirms DM dx

what arethe diagnostic criteria for DM?

less than 100

what is a normal fasting blood glucose level?

pre diabetes

what is an a1c od 5.7-6.4% considered?

diabetic diet

moderate exercise

blood sugar monitoring with insulin replacement-sq

routine follow ups and blood testing

what are the treaments for type 1 dm?

complex carbs, protein, fiber

what are the compnents of a diabetic diet?

diabetic diet and regular exercise

ola medication to stimulate insulin release adn reduce insulin resistance

insulin replacement with sq

what are the 3 levles of control for type 2 diabetes?

3 levels of control diet, exercise, oral meds, insulin replacement

blood sugar monitoring as ordered

routine follow up and blood testing

what are the treatments for type 2 diabetes?

hypoglycemia

diabetic ketoacidosis

hyperosmolar

hyperglycemic

nonketotic state

what are the acute complications of DM?

hypoglycemia

a type of dm acture complication

most commonly d/t overdose of insulin

skipping meals after taking insulin

strenuous exercise

vomiting

90% incidcne in caes of type 1 dm

smyptoms d/t low blood surgar level

neurons affected quickly, cofusion, poor cocnetration ,slurred pseech, staggering gait

stimulatin of SNS, tachycardia, pale, diaphoretic, anxiety, decreased level of consciousness

what are the s/s of hypoglycemia

immediate glucose replacement if related, seizures, coma, and death

what is the tx of hypoglycemia?

diabetic ketoacidosis

acute complication of dm

result of insifficient insulin in the blood high blood glucose levels

most common in type 1 dm

sepsis

sickness

stress

skipping insulin

stuffing yourself

what are the causes of diabetic ketoacidosis?

deficit of insulin,- lack of glucose inthe cells - catabolism or fats/proteins-excessive amounts of fatty acids and metabolites in the body

lack of glucose in the cells leads to catabolism of fats/proteins-excessive amountso f fatty acids and metabolites in the blood

ketones bind with hco3 in the blood-reduction in free hco3-decreases ph=metabolic acidosis

ketones are excreted by kidneys=ketouria but state of dehydration slows excretion leading to severe ketoacidosis=diabetinc ketoacidosis

describe the pathology of dka

r/t metabolic acidosis, dehydration, electrolytes imblances=severe dehydration

acetone breath

increase hr

kusskauls respirations

lethargy decreased reposnisveness

hyperkalcemia

what are the s/s of DKA?

kussmaulsrespirations

lungs are trying to compensate for the extra acid in the body and treis to. get rid oif ti by increasing rr

prolonged acidosis hydrogen in the clel adn k out of the cell and into the blood. insulin helps push the k into the blood and if someone is not takign thier insulin them more k in the blood

why does hyperkalcemia occur with DKA/

insulin

fluid and electrolyte replacement

bicard to correct acidosis

what is the tx for DKA?

all related to chronic high blood glucose levels

microangiopathy

macroangiopathy

infection

what arethe chronic complications of DM?

adrenal or pituitary adenoma

carcinomas

iatrogenic causes

what are the causes of cushing’s syndrome?

autimmune destruction of the adrenal gland most cmmon cause

lack of feedbakc inhibition

ACTH high

what are the causes of addison’s disease

small weka tan

everything is low

low bp, na, weight, glucose, energy, temp, hair

2p’s increased: pigmentations of the skin and increased potassium

what are the s/s of addison’s disease

big round hairy

everthing is big

increased bp, na, weight, glucose

big face

buffalo hump

big belly

big hair

big stretch marks

increased risk for infection

what are the s/s of cushing’s syndrome?

TRH by the hypothalamus

TSH by naterior pituitary

t3 and t4 by the thyroid

what controls the thyroid hormones?

autoimmune process that damages the thyroid gland -hashimotos disease

what is the cause of primary hypothyroidism?

def. if the hypothalamus or pituitary often due to an adenoma or tumor

what is the secondary cause of hypothyroidism?

due to iodine def. in the maternal diet, or genetic defect

what is the congnetical cause of hypothyroidism

t3 and t4 are low

tsh is high=thyroid gland issue

tsh low=adenoma

describe the labs of someone who has hypothyroidism

autimmune process causes thyrid to produce excess t3 and t4=graves disease

more common in women

30-40 yo

what is the primary cause of hyperthyroidism?

adenoma

what is the secondary caue of hypoerthyroidism?

t3and t4 elevated

tsh low=thyroid gland

tsh high=adenoma

describe the labs that are present with hyperthyroidism?

low nad slow

low metabolism of all cells

lowe energy, lethargic, fatigued

low gi motility, low temp, low reflexes

what are the s/ of hypothyroidism?

high and hot

high evergy, nervous, anxious, restless, high hr and bp

high gi motility

high reflexes

great big eyes

what are the s/s of hyperthyroidism?

levothyroxine, medication to replace thyroid hormone t4

what is the tx for hypothyroidism?

radiactive iodine to destroy goiter

removal of the thyroid gland

what is he tx for hyperthyroidism?

aterialblood gas used becaues venous blood gases are highly variable

what is the lab test to access acid base balance?

ph

paco2

hco3

what are the 3 mai nvalues assessed with ABC lab test?

paco2

measure of partial pressure of co2 dissolved in the arterial blodo plasma

35-40 mm hg

reflects respiratory function

hco3

meausres the amount of bicarbonate in the arterial blood

22-26 meq/l

reflects kidney function and gi function

assess ph level

assess the paco2 level

assess the hco3 level

ROME

how do we evaluate an abg?

compensaition

body’s attempt to normalize ph

compensates wit the opposite system

metabolic issue

respiratory issue causing the imblaance

check ph

check the opposite system affected

compensated=ph normal and both the paco2 and the hco3 are still abnormal

uncompensated= ph abnormal and system supposed to be compensating is normal

partially compensated= ph, paco2 and the hco3 abnormal

how do we check for compensation?

respiratory acidosis

increase in co2 level, decreased ph, more acidic high hydrogen elevel

lugns causing the problem and cant compensate for the issue

acute problems ways the body hols on to co2 are not breathing well

pneumonia, airway bostruction, chest injuries

chronic respiratory acidosis= copd

what are the causes of respiratory acidosis?

kidneys = increase excretion of h+, conserve hco3

retaingin co2 =decreased ph

acidic urine

what is the compensation for respiratory acidosis?

metabolic acidosis

excessive loss of bicarb ions= decreased bicarb

decreasedin ph

related to metabolism

diarrhea

hypermetabolism

sepsis

hyperkalemia

salcylate

renal disease or failure wha

what are the causes of metabolic acidosis?

lungs increase rr to get rid of acid, depp and rapid

kidneys: increase excretion of h+, conserve hco3 bicarb, trying to get balance back into normal range

what is the compensation mechanism for metabolic acidosis?