Chapter 14: Coagulopathies and Chapter 16: Hypertension

coagulation disorders

result from problems with thrombocytes (platelets)

thrombocytopenia

low platelet count (can result from too few platelets or from platelets with an abnormal structure or function)

types of thrombocytopenia

1. idiopathic (immune) thrombocytopenia purpura (ITP)

2. thrombotic thrombocytopenic purpura (TTP)

3. heparin-induced thrombocytopenia (HIT)

4. disseminated intravascular coagulation (DIC)

(first 3 are the primary types)

immune thrombocytopenia purpura (ITP)

• most common type of acquired thrombocytopenia

• abnormal destruction of circulating platelets

• typically follows viral infections

• considered an autoimmune disease

thrombotic thrombocytopenia purpura (TTP)

• uncommon

• seen mostly in adult women 20-50 years old

• has 2 types

  • familial: rare, chronic, reptile, may affect children, responds to treatment

  • acquired: more common, acute and sever, affect women in 30’s, rare in infants and elderly

• may be idiopathic: autoimmune disease

• may be due to drug toxicity: chemotherapy

• may be due to pregnancy, preeclampsia or infection

familial TTP

rare, chronic, may affect children, responds to treatment

acquired TTP

more common, acute and severe, affect women in 30’s, rare in infants and elderly

disseminated intravascular coagulation (DIC)

condition characterized by excessive bleeding associated with excessive clotting (often a complication of other diseases or disorders)

• often seen as a complication of pregnancy

• an acute event that occurs simultaneously with other physical diseases or disorders

• most common condition associated with DIC = infectious disease (sepsis) and bacterial infections (gram neg and positive)

• other predisposing conditions: shock, hemolytic processes, obstertric conditions, malignancies, tissue damage

common condition associated with DIC

infectious diseases (sepsis)

bacterial infections (gram neg and pos.)

heparin induced thrombocytopenia (HIT)

• most common drug induced thrombocytopenia

• 4% of people who receive unfractionated heparin will be affected

• caused: surgical procedures and IgG antibodies against heparin plated factor 4 complex

general pathophysiology of thrombocytopenia

• sudden severe, or prolonged reductions in # of platelets can lead to problems with hemostasis that present as increased bleeding from minor injuries to sudden bleeding without injury

• an increase in breakdown of platelets leads to most frequently seen forms of thrombocytopenia: HIT, ITP, TTP, DIC

pathophysiology of ITP

• autoimmune disease: platelets are covered with antibodies

• antibodies are seen as foreign and destroyed by macrophages

• chronic ITP has gradual onset and may see transient remissions

• decreased platelet production or infections or viral infections may add to ITP

pathophysiology of TTP

a life threatening disorder impacting multiple body systems, that causes tiny blood clots to form throughout the body’s small blood vessels

• characterized by

  • thrombotic micoangiopathy - formation of blood clots in small blood vessels

  • ADAMTS13 - enzyme in blood that helps to prevent excessive clotting, activity is severely reduced and vWF proteins are not broken down properly leading to excessive clotting

pathophysiology of HIT

• platelet factor 4 (PF4) is the factor that binds to heparin

• then binds to platelet surface, leading to release of more PF4, resulting in feedback loop

• antibodies form against this complex, leading to early removal from the circulation = decreased number of platelets

pathology of DIC

1. something triggers excessive clotting

2. tiny blood clots form everywhere (too much thrombin that converts fibrinogen into fibrin = helps form blood clots)

3. blood clots block circulation (in capillaries)

4. the body runs out of clotting supplies, (uses platelets, fibrinogen etc), increased clotting stimulates the fibrolytic system

5. excessive bleeding occurs (fibrinolysis is activated, the system that breaks down new clots)

6. system created fibrin split compounds that degrade fibrin, compounds have anticoagulant properties = blood can no longer clot

abnormal clotting cascade

(general process)

1. trigger - sepsis, trauma, cancer, tissue injury

2. clotting system becomes overactive

3. tiny blood clots form throughout the body

4. clots block blood flow - organs do not receive oxygen = organ damage / failure

5. clotting supplies get used up = excessive bleeding

thrombin

causes thrombosis (formation of a blood clot inside a blood vessel)

thrombosis

formation of a blood clot inside a blood vessel

hypertension

type of cardiovascular disorder / vascular disorder: condition where individual has persistently high BP due to specific factors that cause the BP to be elevated (symptoms can be silent)

• exists when systolic pressure is greater than or equal to 140 or diastolic pressure is greater than or equal to 90

hypertensive crisis

extremely elevated BP and characterized by SBP of 180 or higher or DBP of 110 or higher

3 characterizations of hypertension (according to etiology)

1. primary / essential HTN

2. secondary HTN

3. malignant HTN

primary (essential) HTN

(idiopathic - no known cause)

• BP is consistently above 140/90 for average adult

• high BP is not cause by any underlying conditions or medication

• if left untreated over long period of time, it can damage the arterial walls as result of increased vasoconstriction

secondary HTN

it results from another disorder, such as renal (renal artery stenosis) or endocrine (pheochromocytoma) diseases

• the underlying problem must be treated to decrease and manage BP

malignant HTN

• also called resistant hypertension

• severe form of HTN that has many complications

• rapidly progressive and uncontrollable when treated with 3 or more drugs

prevalence of primary HTN

• age, gender, race affect prevalence of HTN

• incidence of HTN increases with age

• more prevalent in men than women until 55 years (menopause increases women’s risk > men

• african americans gave higher prevalence

etiology of primary HTN

lifestyle and hereditary factor HTN

• high sodium diet, alcohol, obesity, stress

pathophysiology of primary HTN

• HTN begins with genetics + lifestyle factors + abnormal BP regulation and then decreased blood flow to kidney

• then an increased production of renin

• then increase causes

  • systemic vasoconstriction - increase peripheral resistance (blood vessels narrow)

  • aldosterone secretions - increased blood volume (kidneys retain sodium and water)

• this combination of both leads to increase in BP

pathophysiology of secondary HTN

causes are renal artery stenosis and pheochromocytoma

1. Underlying disease (e.g., kidney disease)

2. Fluid retention and/or abnormal hormone activity

3. Increased blood volume or blood vessel constriction

4. Increased blood pressure

renal artery stenosis

decreased blood flow to the kidney stimulates production of renin = production of angiotensin II and hyperaldosterone

• angiotensin II causes vasoconstriction

• hyperaldosterone = increased retention of sodium and water

pheochromocytoma

benign tumor of the adrenal medulla produces excess norepinephrine = vasoconstriction and increased HR

• both increase BP

• increased HR increased BP through an increase in cardiac output

clinical manifestations

initial symptoms - fatigue, malaise, headaches in the morning

(primary sign = consistently elevated BP)

which HTN is asymptomatic

primary / essential HTN

• has to be screened for in all patients when they visit their HCP (why its referred to as the silent killery

which statement describes the cause of heparin induced thrombocytopenia

HIT is a drug induced thrombocytopenia

which predisposing factors related to disseminated intravascular coagulation are related to tissue damage

• burns

• severe head injury

• acute anoxia such as after cardiac arrest

which is the most commonly seen acquired thrombocytopenia

immune thrombocytopenia purpura

which infection is the most frequent precursor to disseminated intravascular coagulation

gram negative bacterial

which statement describes a differentiating factor between ITP and TTP

ITP typically follows a viral infection, while TTP is often related to pregnancy

which factor among the forms of thrombocytopenia is seen only in DIC

excessive clotting

which are accurate statements regarding quantitive and qualitative platelet abnormalities

• qualitative abnormalities prevent platelets from forming clots

• quantitative abnormalities reflect a decrease in the number of platelets

• qualitative abnormalities include problems with the structure of circulating platelets

which statement describes the serious impact of TTP

clumping of platelets blocks arterioles and causes ischemia to organs

which statement characterizes the process occurring with HIT

• HIT causes platelet destruction

• HIT results in decreased number of platelets

• HIT requires more heparin to maintain normal ATP levels

• HIT is an immune response to the administration of heparin

which statements are true regarding the pathophysiology of thrombocytopenia

• patients may bleed excessively from minor injuries

• patients may bleed suddenly without any evidence of injury

• all forms of thrombocytopenia lead to a decrease in the number of circulating platelets

which clinical manifestation is most commonly seen in thrombocytopenia

bleeding from the nose or skin

which integumentary manifestation are indicative of DIC

• brusing

• gangrene

• petechiae

• bleeding from previous puncture sites

which statement accurately describes a superficial ecchymosis

large, painful, purple bruises

which central nervous system symptom might be commonly seen with DIC

• seizures

• confusion

• change in level of consciousness

which type of thrombocytopenia presents with memory disturbances

TTP

which obstetrical condition is frequently associated with DIC

placenta abruption

which risk factors are associated with DIC

• burns

• shock

• transfusion reactions

which factor would predispose a patient to chronic DIC

• cancers

• liver disease

• autoimmune disease

in TTP which statement describes the effect on the von willebrand clotting factor (vWF)

ADAMST13 is a plasma enzyme that breaks down vWF and interferes with the adhesion of platelets to damaged endothelial cells

which is an accurate statement regarding the pathophysiology of DIC

DIC is not a disease, but a problem with the clotting cascade

which are accurate statements regarding ITP

• bacterial infections can worsen ITP

• ITP may become chronic with periods of transient remission

• ITP is an autoimmune disorder where the platelets become covered by antibodies and seen as foreign by the immune system

which are accurate statements regarding the fibrinolytic system during DIC

• the fibrinolytic system begins to break down new clots

• the system creates fibrin split compounds that degrade fibrin

which triggers could initiate the clotting cascade in DIC

• trama

• necrosis

• malignant tumors

which clinical manifestations would be associated with gastrointestinal involvement with DIC

occult bleeding

which clinical maifestation is most likely to be associated with heparin induced thrombocytopenia

deep vein thrombosis

infarctions are commonly seen in thrombocytopenia. in which disorder would a practitioner anticipate a myocardial infarction

HIT

which respiratory manifestations would be associated with DIC

• cyanosis

• tachypena

• hypoxemia

which are often the indicators of hemorrhage (excessive blood loss) occurring as a complication of thrombocytopenia

• weakness / fatigue

• pale skin coloring

• drop in hematocrit

• dizziness upon standing

which describes the incidence of hypertension in the US

33% of people have HTN

which classifications of hypertension are considered subtypes that are based on etiology

1. primary HTN

2. secondary HTN

3. malignant HTN

which factors cause secondary HTN

1. renal artery stenosis (having a renal disease)

2. being diagnosed with certain endocrine disorders

which factors are associated with primary HTN

1. obesity

2. high intake of salty foods

3. large consumption of alcohol

4. prolonged or recurrent stressa

which blood pressure screening result for an adult patients, on two separate occasions over a 24 hour period supports a diagnosis of HTN

140/90 mmHg

which is the location where renin is produced

juxtaglomerular cells of the kidney

which triggers the utilization of angiotensin converting enzyme (ACE) in the lungs

angiotensin I

which is the initial step in the development of HTN

decreased blood flow to the kidney

which condition is characterized by a benign tumor of the adrenal medulla and a cause of secondary HTN

pheochromocytoma

which organs can be damaged by persistent HTN

• eyes

• brain

• heart

• kidneys

which are nonspecific symptoms of HTN

• fatigue

• malasie

• headaches

which describes how hypertension is detected

blood pressure screening performed

which are considered to be risk factors in the development of hypertension

1. diet high in processed foods / high sodium

2. high levels of work related stress

3. drinking consumption of 3-4 servings of alcohol

4. increased body weight / BMI

which advice is important of an individual with primary HTN

manage stress levels

which description of malignant hypertension is accurate

it is rapidly progressive

which effect does renal artery stenosis have on BP

stimulates the production of renin

in renal artery stenosis which effect does decreased blood flow to the kidney have

stimulates the production of renin

which is produced in excess in the presence of pheochromocytoma

norepinephrine

which conditions can result from untreated or persistent HTN

• angina

• retinopathy

• nephrosclerosis

• cerebral aneurysm

• myocardial infarction

what are non specific symptoms of HTN

fatigue, morning headaches

which organ is affected if nephrosclerosis develops as a result of untreated HTN

kidney, is a progressive kidney disease