exam2 Flashcards
hyponatremia
sodium less than 135
WATER RETENTION
third-spacing, CFH, liver failure, kidney failure, pneumonia, overhydration, SIADH, hypothyroidism, addison’s disease
-low sodium triggers ADH release
Manifests: CNS deterioration, fingerprint edema, irritability, headache, confusion, muscle weakness, seizures
hypernatremia
sodium greater than 145
DEHYDRATION defective thirst (adipsia or hypodipsia)
Diabetes Insipidus-lack of ADH-failure of kidneys to respond to ADH and vasopressin
Manifests: Thirst, CNS deterioration, Increased interstitial fluid, edema, lethargy, weakness, irritability, neuromuscular excitability
Hypokalemia
potassium less than 3.5
nutritional deficit
excessive renal losses
excessive GI losses
Insulin as treatment for diabetic ketoacidosis, alkalosis (metabolic or respiratory)
Manifests:
bradycardia, ECG changes, CNS changes, Fatigue, constipation, elevated bp
hyperkalemia-seldom occurs in healthy people as the body is very efficient in clearing excesses
potassium above 5 mEq/L
MEDICAL EMERGENCY–ARRYTHMIAS
WANT TO STIM URINATION OR DO DIALYSIS TO TREAT
metabolic acidosis
addisons disease
tissue trauma, burns, crushing injuries, extreme exercise, seizures, renal failure, some diuretics, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers
hypocalcemia
calcium less than 9 mg/dL
hypercalcemia
calcium greater than 11 mg/dL
Normal Hct
males 40-54%
females 37-47%
indicates level of hydration and oxygen binding capacity
normal BUN
normal BUN 7-20mg/dL
elevated BUN indicates a kidney problem
urea is a by-product of metabolism and is primarily excreted by the kidneys in urine
Elevated bun when gfr and blood volume decrease ( hypovolemia)
Fever, high protein diet, increase catabolism, gi bleeding
Urine Specific Gravity
1.010-1.020
measures the weight of fluid in relation to water (water =1.000)
Normal Na+
Normal Na+ 135-145
water balance
Normal K+
Normal K+ 3.5-5
transmission of nerve and muscle impulses
Normal Cl-
Normal Cl- 104-106
buffer and regulates acid base balance
Normal Ca2+
Normal Ca2+ 9-11
nerve impulse transmission, heart contractions
Normal Glu
normal Glu 80-100
If a patient has a glucose reading of 1490, their first space is dehydrated.
First Spacing
normal distribution of fluid in ICF and ECF (vascular space)
Second Spacing
edema
abnormal accumulation of interstitial fluid
Third Spacing
Ascites
fluid accumulation in part of the body where it is not easily exchanged with ECF
ICF electrolytes
potassium, proteins, phosphates
ECF electrolytes
sodium, chloride, bicarb
Diuretics
pull fluid out of cells increase urine water output hypovolemia hypokalemia hyponatremia metabolic alkalosis metabolic acidosis
albumin
puts fluid back in cells
main protein of human blood plasma
regulates colloidal osmotic pressure of blood compartment
give albumin to patients with —— blood volume to —— them
give ALBUMIN to patients with LOW blood volume to REHYDRATE them
ADH function
trigger-dehydration
Antidiuretic hormone functions to increase water reabsorption. You retain water and recirculate blood volume. your urine is more concentrated and dark. vasocontrictor/vasopressin, water retention
increases blood pressure
overproduction of SIADH
syndrome of inappropriate adh
ADH is OVERPRODUCED
leads to FLUID RETENTION and EDEMA
leads to hyponatremia
what stimulates release of ADH?
low sodium levels
resultant water retention and sodium loss together cause HYPONATREMIA a key feature of SIADH.
ANP
counteracts ALDOSTERONE, inhibits ADH
released by muscle cells in the atria in response to high blood volume (increased atrial pressure). Function is to REDUCE SODIUM, WATER, AND ADIPOSE cells in circulation thereby REDUCING BLOOD PRESSURE-vasodilation
effect of angiotensin II
aldosterone
retain sodium and water, INCREASE BP
excrete potassium
low blood volume/pressuer sitmulates release of aldosterone from adrenal cortex
RAAS
regulates long term blood pressure and ECF volume. Angiotensinogen from liver triggers cascade response when blood pressure and sodium concentrations are low. Resultant vasoconstriction leads to release of aldosterone=sodium and water retention=increased BP.
Overhydration
ACIDOSIS
cyanosis, shock, CHF, neck vein distension, full, bounding pulse, ELEVATED BP, weight gain, PULMONARY EDEMA
Dehydration
dry mucous membranes, sunken eyeballs, weight loss, increased RR, decreased skin turgor, increased HR, DECREASED BP, hypernatremia
hypovolemia
decreased blood volume typically due to hemorrhage or dehydration
Normal Blood Volume
280-300mOsm
Hypertonic IVF
draws water out of the cells to reduce edema
prolonged fever, tube feedings without enough water
impaired thirst
Hypotonic IVF
puts water back in the cells and they plump up
renal losses, malnutrition, GI losses
lack of ADH
diabetes insipidus
Normal Hemoglobin
female 12-16 g/dL
males 12-18 g/dL
What would a hemoglobin reading of 9 indicate?
A hemoglobin of 9 is low for both sexes and indicates a reduced oxygen carrying capacity. Result anemia and maybe tissue hypoxia. Tissue hypoxia gives rise to fatigue, dyspnea, and sometimes angina. Brain tissue hypoxia causes headaches, faintness, and dim vision. The lack of hemoglobin causes pallor of the skin, mucus membranes, conjunctiva, and nail beds. Tachycardia and palpitations may occur as the body tries to compensate for the reduced O2 with increased cardiac output. Ventricular heart hypertrophy and high output heart failure may develop in persons with severe anemia, particularly those with pre-existing heart disease. All the listed features above would be increased by an even lower hemoglobin level of 4 g/dL.
why is the spleen so important in terms of hematology?
The spleen contains phagocytic cells that recognize and destroy old and defective RBC’s. It breaks down the hemoglobin into heme and globin. The heme goes either to bone marrow to be reused, the liver or spleen for storage, or is secreted in bile to either be excreted as feces or urine.
Hemophilia signs, symptoms, clinical features
sex-linked, inherited bleeding disorder, results in deficiency of factor VIII or IX.
Manifested by hemorrhage into various body parts. Bleeding usually occurs in soft body tissues, GI tract, hip, knee, elbow, and ankle joints. Medical management includes FFP transfusion, recombinant clotting factors
Leukemia
uncontrolled proliferation of WBC’s in the bone marrow.
Acute leukemia
cancers of hemaopoietic progenitor cells. Usually a sudden and stormy onset with signs and symptoms related to depressed bone marrow function.
Acute lymphocytic leukemia
most common leukemia in children and adults
chronic leukemia
malignancies involving proliferation of more fully differentiated myeloid and lymphoid cells. Primarily a disease of old age. Average diagnosis age 67. Rarely seen in people younger than 40.
Pancytopenia
reduction in ALL CELLULAR ELEMENTS of BLOOD
RBC, WBC, platelets
Cause of pancytopenia
complete bone marrow failure-congenital chromosomal alteration
exposure to benzene ionizing radiation, chemical agents, severe viral and bacterial infections
Chemo can be a cause of pancytopenia
pernicious anemai
vit b12 deficiency related to a lack of intrinsic factor.
Must give vit b12 IM to treat
Where is intrinsic factor made
parietal cells at top of stomach
What does vit b12 do in the body
it is needed to manufacture and mature RBC’s
Treatment of anemia
based on etiology dietary and injections/infusions-pernicious and folate deficiency iron supplementation-iron anemia splenectomy-hemolytic anemias corticosteroids
Treatment for sickle cell anemia
avoid sickling episodes-infections, cold exposure, severe physical exertion, acidosis, dehydration.
May require blood transfusionsO2: Begin with 2L
IVF: Begin with NS boluses and anchor a FC if needed
PRBC: Usually 2 units red cells given to combat hemolysis and raise H&H
Hydroxyurea:Antineoplastic used to treat sickle cell disease that may help your body make RBC’s that are less likely to sickle. may also help prevent a CVA.Not on exam
Bronchodilators:This medicine is used to help dilate the airway.
Steroids:Steroid medicine may be given along with pain medicine. It may help decrease the amount of pain that you are having. It can also make the pain go away sooner.
IVPCA: Morphine sulfate, Dilaudid, Ketamine
pulmoary embolus
respiratory alkalosis
hypotension
meabolic acidosis
vomiting
metabolic alkalosis
sevee diarrhea
metabolic alkalosis
cirrhosis
respiratory alkalosis
renal failure
metabolic acidosis
sepsis
respiratory alkalosis, metabolic acidosis
pregnancy
respiratory alkalosis
diuretic use
metabolic alkalosis
COPD
respiratory acidosis
drugs that increase preload
vasodilators
nitroglycerin (NTG)
Drugs that increase afterload
vasoconstrictors
epi, dopamine, levophed
what to do for hypertension and chest pain?
reduce preload!
What to do for low blood volume?
increase preload!
sympathetic stimulation of heart
increase inotropy, filling pressure, resistance, and blood pressure
decrease volume
vasoconstriction
Parasympathetic stimulation of heart
return to homeostasis
low and slow
cranial nerve 10-vagus nerve
right sided heart failure
cor pulmonale-pulmonary heart disease
caused by chronic high blood pressure
lung hypoxia, COPD, cystic fibrosis
left sided heart failure
CHF, back up happens in the lungs, caused by HBP or heart muscle defects, valve defects
Pre-hypertension
bp 120-139 mm HG (80-89 mm HG)
treat with diet and lifestyle changes
lower sodium and fat, increase potassium
exercise 30 min/day, healthy weight, no smoking, decreased alcohol comsumption
Hypertension
140/90
Inflammation, endothelial dysfunction, obesity-related hormones, , and insulin resistance also contribute to both increase peripheral resistance and increase volume.
Increased volume = decrease in renal excretion of salt, often referred to as a shift in the pressure-natriuresis relationship – meaning they excrete less salt = EDEMA
SNS increases production of epi & norepi = increasing heart rate and vasoconstriction and angiotensin levels and pro-coagulation effects.
why give diuretics to treat hypertension?
This type of high blood pressure medicine helps your kidneys remove salt and water from your body. One of the results is that you have less blood volume circulating in your blood vessels. Less volume in the vessels leads to lower blood pressure
Why give beta blockers to treat hypertension?
This type of high blood pressure medicine makes the heartbeat slow down. Beta-blockers also keep your heart from pumping so hard. This makes blood go through your vessels with less force. The pressure inside your blood vessels goes down. Acts on sympathetic nervous system
ex albuterol
how do Alpha-blockers treat hypertension?
This type of high blood pressure medicine reduces nerve impulses that tell your vessels to tighten. Your blood vessels remain relaxed, lowering your overall blood pressure.
counteract epi
how do ACE inhibitors treat hypertension?
ACE inhibitors – angiotensin-converting enzyme inhibitors – are a type of high blood pressure medicine prevents your body from making angiotensin II. Angiotensin II is a hormone that makes blood vessels tighten. Because ACE inhibitors lower the amount of this hormone in your body, your blood vessels remain relaxed. Blood flows more easily through the vessels, lowering your overall blood pressure.
cardiogenic shock
heart fails to pump sufficiently to meet the body’s demands
Decreased CO, hypotension, tissue hypoxia (even though intravascular volume is normal)
Aortic Valve Stenosis
Most common valve disorder
calcification
replace valve
can cause CHF, angina, alterations in BP, arrhythmias
COPD
chronic obstructive pulmonary disorder
caused by smokin,g pollution, genetics
symptoms: shortness of breath, cough, sputum, easily fatigued, wheezing, finger clubbing
Pleural effusion
an abnormal collection of fluid in the pleural cavity
Transudative effusion
serous transudate (clear fluid) in the pleural cavity aka HYDROTHORAX most common cause=CHF
Exudative effusion
accumulation of pleural fluid that has a specific gravity greater than 1.02 and contains inflammatory cells.
pneumonia, cancer, lymphoma
Hemothorax
BLOOD in pleural cavity
Empyema
PUS in the pleural cavity
Chylothorax
lymphatic fluid (chyle) in the pleural cavity lymphoma or thoracic surgery
cor pulmonale
(right sided heart failure)
enlargement and failure of right ventricle due to increased vascular resistance and HBP in lungs
Pneumothorax
presence of air in the pleural space
spontaneous pneumothorax
rupture of an air filled bleb or blister on the surface of the lung
traumatic pneumothorax
injury-fractured rib is most common
Tension pneumothorax
intrapleural pressure exceeds atmospheric pressure, occurs when injury to chest permits air to enter but not leave the pleural space.
ARDS- acute respiratory distress syndrome
sudden form of respiratory failure characterized by acute inflammation
injury to the pulmonary capillary endothelium
inflammation and platelet activation
Atelectasis-collapse or closure of lung
Causes of ARDS
infection trauma aspiration shock-sepsis fat emboli
digoxin
treat CHF
+ INOTROPE
Slows HR, but strong contractions
Na+/Ca+ exchange
Increases intracellular calcium levels which, in myocardial muscle, enhances the force of contraction
Blocks atrioventricular (AV) conduction and slows heart rate by enhancing vagal nerve
ischemia
imbalance between myocardial oxygen supply and demand=hypoxia
a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism
what causes ischemia?
decreased blood flow to the cardiac muscle secondary to arterial atherosclerotic blockage
What are the potential consequences of ischemia?
poor cardiac pumping
cardiac rhythm changes
chance of an mi
causes of ischemai
cad
thrombus formation
coronary artery spasms
sepsis-severe illness-body’s metabolic demands are greatly increased and BP is too low to pump effectively.
infarction
tissue death caused by a local lack of oxygen
atherosclerosis
plaque in arteries made from foam cells (body armour) typically found in aorta and its branches, to remove, we must scoop it and suck it out.
clinical manifestations of Ischemia
angina pectoris-lactic acid buildup dyspnea nausea weakness diaphoresis (sweating) zanthelasma (cholesterol deposits over eyes) Arcus similis (halo on iris-NEVER normal in kids) tacharrythmias (pumping problem)
Classic symptom of ischemia that is indicative of a CAD?
Angina pectoris!!
what are three kinds of angina?
Stable (predictable) give NTG
unstable-ALWAYS A MEDICAL EMERGENCY
variant-Prinzmetals’s-exclusively happens in the middle of the night
Which type of Angina is ALWAYS a medical emergency?
unstable
could be an MI, acute Coronary syndrome
its an emeergency-call 911, EKG, Aspirin, Trops, to the Cath lab!!
what labs do you run for an unstable angina?
EKG
Trops-immediate, 6 hrs, 6 hrs >.1 goes to cath lab!
PCI
stress test
Explain the PCI process
Cardia Catheterization
give NTG-blood thinner to keep blood moving
physician puts an angiocatheter into your artery. Needle has a wire and threads it all the way to the arteries outside of the heart. Taking pictures and injecting dye the whole time. Complete blockage leads to MI, partial blockage leads to ischemia
Stem vs Non stemi
ST segment elevation=heart attack
Coronary artery is completely blocked off
profoundly life threatening as the blood clot has cut off blood supply to heart muscle. usually assoc. with atherosclerosis
No ST elevation. When blockage of the coronary artery is not complete, so that a relatively small portion of the heart muscle is becoming damaged. Stiall an MI and still taken seriously.
which lab is the gold standard for detection of an MI?
Troponin. a negative result is .01 or less. a positive result is greater than .01
the test must be performed THE DAY the patient arrives at the hospital because it is time sensitive
what lab besides the trops is useful for detection of an mi?
LDH if patient is admitted for chest pain but had symptoms a few days ago. LDH levels rise 24-72 hours after symptoms.
what is the biggest risk when having a PCI>
thrombosis-blood clot dislodged by the stent
What are stents for?
Stents are placed into the coronary arteries to open them up and improve blood flow, relieve chest pain, and improve chances of surviving an MI (increase collateral pathways)
What happens if a patient has too many stents?
CABG-coronary artery bypass graft
revascularization process in which a blood vessle is taken from elsewhere in the body and surgically sutured around a blocked coronary artery.
Sickle cell crisis in african americans. why?
autosomal recessive trait most commonly found in african americans. once of the biggest concerns would be blood clots.
If platelets were under 100,000 what would we be concerned about? what about under 50,000? What if platelets fell to 10,000?
Thrombocytopenia-spontaneous bleeding may occur at levels 10,000-20,000.
The lower your platelet count, the greater your risk of bleeding. The higher the platelet count, the more clotting.
Normal platelet?
150,000-400,000mm3
iron deficiency anemia
hypoproliferative
most common due to poor diet
inadequate iron intake or malabsorption
blood loss without fast enough uptake
macrocytic normochromic (megaloblastic) (hypoproliferative)
Ineffective erythropoiesis 2° B vitamin deficiency
Characterized by defective DNA synthesis
Large stem cells in the bone marrow called megaloblasts mature into odd large and fragile erythrocytes
Cells die prematurely resulting in elevated bilirubin levels
CBC characteristics
Absolute anemia
Abnormally large RBC
Normal color
megaloblastic cobalamin B12 deficiency
Pernicious Anemia
(hypoproliferative)
Cobalamin Deficiency—aka, pernicious anemia Vitamin B12 (cobalamin) is an important water-soluble vitamin Intrinsic factor (IF) is required for cobalamin absorption Causes of cobalamin deficiency: Gastric mucosa simply stopped secreting/manufacturing IF = Crohn’s Gastric bypass vs sleeve Long-term use of H2 receptor blockers cause atrophy of gastric mucosa and decrease in parietal cell numbers Nutritional deficiency Hereditary defects of cobalamin utilization Indirectly r/t ETOH abuse and gastric parietal cell destruction
megaloblastic Folic Acid (B9) Deficiency
hypoproliferative
ETOH HD Chemotherapy (Methotrexate) and Antiseizure Dilantin HIV/AIDS Antivirals Poor dietary intake or malabsortption
Chronic Disease Anemia
hypoproliferative
Underproduction of RBCs, shortening of RBC survival
2nd most common cause of anemia (after iron deficiency anemia and is r/t INFLAMMATORY RESPONSE
Generally develops after 2 months of sustained disease
Causes: Chronic inflammatory, infectious and malignant disease
Long-term HD
Chronic Folic acid deficiencies
Splenomegaly
Hepatitis
AIDS
Crohn’s
Cancer
The anemia is most often normochromic and normocytic with low reticulocyte count
ABNORMAL IRON METABOLISM
Enough iron, just impaired release of iron
Reduced concentration of transferrin
Treat with transfusions and procrit injections
Aplastic Pancytopenia
hypoproliferative
decrease of all blood cell types
Complete bone marrow failure
Intrinsic Anemia
Hemolytic
Intrinsic hemolytic anemia
Abnormal hemoglobin
Enzyme deficiencies
RBC membrane abnormalities that make is easy to break down
Hemolytic anemia
Anemias caused by increased erythrocyte destruction
Destruction or hemolysis of RBCs at a rate that exceeds production= HIGH RETICULOCYTE COUNT + JAUNDICE
Third major cause of anemia
extrinsic anemia
Hemolytic
Extrinsic hemolytic anemia
Normal RBCs but…
Damaged by external factors
Liver problems
Hypersplenism = Enlarged and over-stuffed
Toxins= chemo, radiation, transfusion reaction, medication-induced, toxic chemicals
Mechanical injury (mech heart valves)
Hemochromatosis
hemolytic
Over-absorption (from food) and storage of iron causing damage especially to liver, heart and pancreas
Excess iron poisons organs, leading to life-threatening conditions such as cancer, heart arrhythmias & cirrhosis
Hemosiderosis = transfusion-related Fe overload
sickle cell anemia
Hemolytic
Autosomal recessive trait Symptomatic at 6 months of age Irreversible sickling upon deoxygenation pain crises infarcts of spleen, kidneys, brain, heart swollen joints dehydration and clotting risk
alloimmune hemolysis
hemolytic transfusion reaction
Caused by recognition of foreign antigens on transfused blood cells
Several types
Immediate Intravascular Hemolysis (Minutes) - Due to preformed antibodies; life-threatening; Clogs FC and kidneys
Slow extravascular hemolysis (Days) - Usually due to repeat exposure to a foreign antigen to which there was a previous exposure; usually only mild symptoms
Delayed sensitization - (Weeks) - Usually due to 1st exposure to foreign antigen; asymptomatic
Medical Emergency: NS KVO
Vitamin B12
vitamin B-12, also called cobalamin, is a water-soluble vitamin with a key role in the normal functioning of the brain and nervous system, and for the formation of blood. It is one of the eight B vitamins. It is normally involved in the metabolism of every cell of the human body, especially affecting DNA synthesis and regulation, but also fatty acid synthesis and energy production.
Intrinsic Factor
Needed to absorb vitamin B12. Secreted from parietal cells in top of stomach.
DIC Disseminated Intravascular Coagulation
a serious disorder where the proteins that control blood clotting become overactive. Clots form in blood vessels not related to injury-lead to blocked arteries and the use of available clotting factor to treat actual injury-danger of bleeding out.
Combined bleeding/thrombotic disorder
Severity is variable; may be life-threatening
Triggers may include sepsis, trauma, shock, cancer, abruptio placentae, toxins, and allergic reactions, malignancies, liver disease
Altered hemostasis mechanism causes massive clotting in microcirculation; as clotting factors are consumed and lost, bleeding occurs; symptoms are related to tissue ischemia and bleeding
lymphoma
Lymphoma is a type of blood cancer that occurs when B or T lymphocytes,[1] the white blood cells that form a part of the immune system and help protect the body from infection and disease, divide faster than normal cells or live longer than they are supposed to. Lymphoma may develop in the lymph nodes, spleen, bone marrow, blood or other organs[2] and eventually they form a tumor.[1]
Hodgkins Lymphoma
Reed–Sternberg cell diff between hd and NHD
EBV?; familial pattern; incidence occurs in early 20s and again after age 50
Excellent cure rate with treatment
Manifestations: painless lymph node enlargement; pruritus; fever, night sweats, and weight loss
Treatment is determined by stage of the disease and may include chemotherapy and/or radiation therapy
Non Hodgkins Lymphoma
Lymphoid tissues become infiltrated with malignant B lymphocytes that spread unpredictably; localized disease is rare
Incidence increases with age; the average age of onset is 50 to 60
Prognosis varies with the type of NHL
Diagnosed via lymph node biopsy and imaging
Treatment includes interferon, chemotherapy, and/or radiation therapy
Why would a heavy smoker with COPD who requires O2 to live, require only low levels of O2?
They would only require low level of O2 because their level of O2 affinity in the hemoglobin has decreased. This leads to looser bindng to the oxygen and it is therefore unloaded more easily at the tissue level. This signifies a shift to the right on the dissociation curve.
Manifestations: painless lymph node enlargement; pruritus; fever, night sweats, and weight loss
HD Hodgkins Lymphoma
If you entered your patient’s room and found him peacefully asleep breathing about 5 times per minute, on 8L O2, what would you do? Why? What could you anticipate your MD ordering so you could definitively know what was wrong with your patient?
You would WAKE THEM UP, SIT THEM UP to see if their breathing can speed up a little to get rid of some of the CO2 because they are acidotic. Thurn the O2 down. The doctor would order an ABG to find out how severe the problem is and possible ventilate.
ABG pH
normal 7.35-7.45
If its high, its alkalosis
If its low, its acidosis
if its normal, it is FULLY COMPENSATED or NORMAL
ABG CO2
normal 35-45
if it is high, its acidosis (slowwww)
If it is low, its alkalosis (fast fast fast)
ABG HCO3
Normal 22-26
If its high, metabolic alkalosis (lots of bicarb)
if its low, metabolic acidosis (not enough bicarb)
ABG 2 out of 3
acute
ABG 2 high (or low) 1 off in the other direction
partially compensated
hypercapnia slow breathing causes CO2 buildup in blood COPD Ventilated patients sedated people pregnancies pulmonary edema pneumothorax
respiratory acidosis
hyperventilation anxiety people in labor patient with ascites sepsis high altitudes
respiratory alkalosis
most common acid base balance
a problem with the body or kidneys lactic acidosis (usually from cardiac arrest) severe diarrhea diabetic ketoacidosis starvation renal failure sepsis
metabolic acidosis
loss of body fluids vomiting/diarrhea heavy ingestion of antacids severe dehydration high levels of diuretics
metabolic alkalosis
thirst
fluid in interstitial space
CNS deterioration
hypernatremia
sodium greater than 145
lethargy
confusion
difficulty standing
weakness
hyponatremia
sodium less than 135
bradycardia
hypokalemia
potassium less than 3.5
ventricular fibrillation
ECG changes
Nausea
Hyperkalemia
potassium greater than 5
muscle twitching
Chvostek’s sign (face twitches when cheek is touched)
Trousseau’s signs (arm turns in when bp cuff is put on)
Hypocalcemia
calcium less than 9
renal calculi=kidney stones
thirst
increased interstitial fluid
body may be pulling from bones-may have weak bones
hypercalcemia
calcium greater than 11
Effect of anemia on cardiovascular function
increase preload, HR, stroke volume
reduce afterload
effect of anemia on respiratory function
dyspnea
effect of anemia on nervous system
myelin degeneration
effect of anemia on GI
pain
nausea
vomiting
anorexia
Anemia manifestation
reduced oxygen carrying capacity
classic anemia symptoms
fatigue, weakness, dyspnea, pallor
loss of appetite, abdominal pain, beefy red tongue (atrophic glossitis), icterus (jaundice), splenic enlargement
Normochromic-Macrocytic Anemais
pernicious anemia
Most common type of anemia worldwide Nutritional iron deficiency Metabolic or functional deficiency Progression of iron deficiency causes: Brittle, thin, coarsely ridged, spoon-shaped nails A red, sore, painful tongue Symptomtic Hgb 7-8 g/dl
Iron deficiency anemai
hypochromic-microcytic anemias
leukocytosis
increased number of leukocytes
a normal protective physiologic response to stressors
leukopenia
deficiencies in the quality and quantity of leukocytes
always abnormal
neutropenia
reduction in circulating neutrophils
causes of neutropenia
prolonged severe infection
decreased production
reduced survival
abnormal neutrophil distribuation and sequestration
leukemias
overcrowding of bone marrow
decreased production and function of normal hematopoietic cells
anemia, bleeding purpura, petechiae, ecchymosis, thrombosis, hemorrhage, DIC, infection, weight loss, bone pain, elevated uric acid, liver, spleen, and lymph node enlargement
signs and symptoms of leukemias
lymphadenopathy
enlarged lymph nodes tht become palpable and tender
changes in proto-oncogenes and tumor-suppressor genes contribute to cell emmortality and thus an increase in malignant cells
NHLymphoma
thrombocytopenia
Platelet count <10,000/mm3—severe bleeding
Causes:
Hypersplenism, autoimmune disease, hypothermia, and viral or bacterial infections that cause DIC
vitamin K deficiency
Vitamin K is necessary for synthesis and regulation of prothrombin, the prothrombin factors (II, VII, XI, X), and proteins C and S (anticoagulants)
Liver Disease
Causes broad range of hemostasis disorders
Defects in coagulation, fibrinolysis, and platelet number and function
what initiates DIC?
endothelial damage leads to
unregulated release of thrombin with subsequent fibrin formation and accelerated fibrinolysis
Low reticulocyte count in an anemic patient may indicate what?
a hypoproliferative disorder
SIADH TOO MUCH ADH
HYPONATREMIA- FLUID RETAINED SODIUM LOST
DIABETES INSIPIDUS- FAILURE TO RESPOND TO ADH
HYPERNATREMIA
High reticulocyte and jaundice
Hemolytic anemia
