Pathophysiology T2 Notes

inflammation…

prerequesite for would healing…

wound healing…

CVA= stroke

stroke is irreversible

• categorized by the cause

  • ischemic (majority of CVAs)

  • hemorrhagic

  • global hypoperfusion

• ischemic CVA

  • what causes it?

    • blockage of an artery leading to the brain

    • ALMOST ALL are due to atherosclerotic plaque

      • causes less blood flow through the vessel

      • plaques can rupture which forms a clot in the vessel

      • the clot blocks blood flow to the brain

  • Who is at risk?

    • diabetics

    • smokers

    • etc

• hemorrhagic CVA

  • what causes it?

    • damage to a vessel that directly supplies the brain

  • who is at risk?

    • those with uncontrolled HTN

    • blunt trauma patients

• global hypoperfusion CVA

  • what causes it?

    • something causing the blood flow elsewhere to be diminished drastically

  • the brain is NOT the only organ impacted by

• clinical manifestations

  • dictated by location and size

    • if the same location, then the size determines the severity

    • if different locations, then size can matter but the specific location is often more important

  • ischemia

    • CAN be reversed IF quick enough to get the blood flow to the area again

    • if ischemia is severe enough then the stroke is worse

• strokes (CVAs) CAN expand, but they CAN’T be reversed

• REMEMBER: ANY brain damage is slow to heal in any brain injury, such as in a head trauma!!! This means that function and cognition CAN be decreased for long periods and then returned. We know it’s NOT a stroke in these cases because the damage was reversible!!!

• Is it blocked?

  • then it’s ischemic

• Is it ruptured?

  • then it’s hemorrhagic

• Is it in ALL the body?

  • then it’s a global issue

TIA= Transient Ischemic Attack

• temporary deficit due to a lack of blood flow

• What makes it different from a stroke?

  • it is REVERSIBLE!!!

• TIAs are often a sign that a stroke can happen later

  • STROKE RISK IS HIGH after a TIA occurs

• How do we treat a TIA?

  • we use the same procedures as we would with a stroke

• REMEMBER: the more acute it is the more immediate the manifestations!!!

TBI= Traumatic Brain Injury

• this is a brain injury secondary to trauma

• what is the most common cause?

  • FALLS: particularly common in ages 1-17 and 55 and older

  • MOTOR VEHICLE ACCIDENTS: specific to the ages of 17-44

• what are the warning signs/broad manifestations?

  • disorientation

  • behavior change

  • lethargic

  • inability to recognize

  • confusion

GCS= Glasgow Coma Scale

• this works as a way to see the severity of damage done to the brain as well as to assess the level of consciousness in a person

• LOC= level of consciousness

• The lowest possible score is a 3

• The highest possible score is 15

• There can NEVER be a GCS of 0!!!

• What are we looking for?

  • Eyes: 1-4

    • 1= the lowest and no response/not opening

    • 4= the highest and a simultaneous response with the eyes opening

  • Verbal: 1-5

    • 1= the lowest and no response

    • 5= the highest and noted as being alert and oriented x4; means the person is alert to person, place, time, and situation.

  • Motor: 1-6

    • This is related to the patient’s response and ability to respond to verbal commands for motion

    • 1= the lowest and no response

    • 6= the highest and can follow motion commands

Endocrine Disorders

• The endocrine system is responsible for hormones

• hormones= chemical messengers

• For hormones to produce their effects, they must interact with a specific receptor

• every hormone has its own targets

  • something is a target if it has the hormone’s specific receptors

• hormones are normally produced ONLY as we need them in the body

• What is Primary versus Secondary disorders?

  • Primary= a gland issue

  • Secondary= problem source outside of the gland

  • FOLLOW THE FEEDBACK LOOPS!!!

  • ASK “Is this the expected response?”

    

ADH= Antidiuretic Hormone

• released from the posterior pituitary into the circulation

• targets the kidneys

• reduces urine output and thus makes water be retained

• also called vasopressin

• what are its major effects?

  • raises blood volume

  • acts as a vasoconstrictor

  • causes water retention

  • ALL these result in raising blood pressure!!!

• Too much ADH is called Syndrome of Inappropriate ADH (SIADH)

• Too little ADH is called Diabetes Insipitus (DI)

SIADH

• What are the effects?

  • too much water retention

    • ECF becomes hypotonic

      • water flows from the ECF to the ICF

      • cells expand

      • possible hyponatremiaia

  • the BV increases so BP increases

• What is our primary concern?

  • the water buildup in the ECF which results in a fluid shift

DI= Diabetes Insipitus

• causes an increased urine output

• there are 2 types:

  • very low ADH

    • CDI= Central DI

      • no hormone being released results in low levels

  • reduced response to ADH

    • is a receptor problem

    • NDI= nephrogenic DI

• How can you tell the difference between the types?

  • do a blood test for ADH levels

    • CDI= very low levels because the hormone isn’t being produced

    • NDI= normal or elevated levels because the hormone is being produced but the body can’t use it due to a receptor issue

• what are the effects?

  • reduction in water retention

  • substantial increase in urine output!

    • also called polyuria

  • extreme thirst

    • also called polydipsia

    • results from peeing off water

  • BV decreases

    • also called hypovolemia

  • BP decreases

    • results from decreased BV

    • also called hypotension

  • ECF osmolarity becomes hypertonic

    • results from water loss

  • Na concentration increase

    • results from water loss

    • also called hypernatremia

  • urine is extremely dilute because of the amount of water being peed off

Example Patient

Complaints of being unable to make it to Fayetteville now because they keep stopping to pee. What could be a possible diagnosis? (List 4)

1. DI (either CDI or NDI)

2. DM (would be most common)

3. intense water increase

4. diuretics

Thyroid Hormone

• thyroxicosis= the excess of TH from any source

  • a common cause is the overproduction of TSH by the anterior pituitary gland

• The anterior pituitary makes TSH

  • stimulates the thyroid gland to release TH

• The thyroid gland makes TH

• “In primary, Mr. Thyroid isn’t listening to Mr. Pit”

• “In secondary, Mr. Pit went ‘off brand’”

Hyperthyroidism

• What is the overall clinical picture?

  • speeds things up…

  • has enhanced effects

  • SNS sensitivity increases

  • metabolism increases

• What are common symptoms?

  • weight loss

  • heat intolerance

  • irritability

  • fatigued

  • increased BP

  • tachycardia

• What is the difference between primary and secondary hyperthyroidism?

  • Primary (1*)= The thyroid gland is the source of the problem

  • Secondary (2*)= Usually the anterior pituitary gland is the source of the problem

    • most commonly caused by a benign tumor on the pituitary

  • THINK: if the TSH is elevated then the TH should be elevated; if the TH is elevated then the TSH should decrease to cause less TH to be created

  • tell the difference by first looking at TH levels and then looking at TSH

• Patient 1:

  • TH elevated

    • means that this patient has hyperthyroidism

  • TSH is at normal or even low level

    • this is the expected response to elevated TH

  • IF the TSH is low then that means the TH is being released with no stimulation from the ant. pit.

  • Abnormal response by the thyroid gland

  • this patient has primary hyperthyroidism

• Patient 2:

  • TH elevated

    • means the pt has hyperthyroidism

  • TSH levels are elevated

    • the thyroid is reacting as expected to the TSH levels and producing more TH

    • ant. pit. problem!!!

  • this pt has secondary hyperthyroidism

Hypothyroidism

• mostly the polar opposite of hyperthyroidism

• the low TH causes a low metabolism

• What are the common manifestations?

  • weight gain

  • cold intolerance

  • fatigue/lethargic

• Patient 1:

  • low TH

    • means pt has hypothyroidism

  • decreased TSH

    • not the normal ant. pit. response

    • would expect the ant. pit. to produce MORE TSH to counter the low TH levels

  • The thyroid is responding normally to the decreased TSH levels

  • pt has secondary hypothyroidism

• Patient 2:

  • low TH

    • means pt has hypothyroidism

  • increased TSH

    • normally response by ant. pit. to low TH

  • thyroid responding abnormally to the increased TSH levels

  • pt has primary hypothyroidism

• Patient 3:

  • increased synthroid (a TH replacement drug)

  • would expect the TSH to decrease

  • we use this response to determine the dose in thyroid replacement therapy

Cortisol

• is the “stress” hormone

• released by the adrenal cortex above the kidneys

Cushing’s Syndrome= Hypercortisolism

• too much cortisol

• often has very noticeable outward manifestations

• what are the common symptoms?

  • muscle wasting

  • humping

  • moon face

  • …

  • …

  • …

• primary hypercortisolism is caused by a problem with the adrenal cortex

• secondary hypercortisolism is caused by a problem with the anterior pituitary

• Patient 1:

  • cortisol elevated

  • ACTH decreased

    • the normal response by the ant. pit.

    • if ACTH decreased, then would expect the cortisol levels to decrease as well

  • problems with the adrenal release of cortisol

  • pt has primary hypercortisolism

• Patient 2:

  • cortisol elevated

  • ACTH elevated

    • abnormal response by the ant. pit.

    • ant. pit. is overproducing ACTH which is causing an abnormal amount of cortisol production by the adrenals

  • problem with the anterior pituitary gland

  • pt has secondary hypercortisolism

  • secondary hypercortisolism= Cushing’s Disease

• CD= Cushing’s Disease

  • specifically caused by the excess of ACTH

• Cushing’s Disease is always Cushing’s Syndrome but Cushing’s Syndrome is not always Cushing’s Disease.

• could be due to giving high doses of steroids

  • would expect a decrease in ACTH as a result of cortisol increase by adding corticosteroid drugs

• treat by discovering the cause and then addressing it

Hypocortisolism

• low cortisol production

• can be primary or secondary

• REMEMBER: cortisol is a stress hormone

  • means that there is a suppressed stress response in hypo

• in primary, there is a problem with the adrenal cortex so the ACTH is elevated because it is trying to tell the adrenals to make cortisol but they are not

• in secondary, there is a problem with the anterior pituitary so the ACTH is decreased which means the adrenal cortex is not being stimulated to make cortisol

• NORMAL FEEDBACK

  • ACTH decreased

  • cortisol decreased

  • ACTH increased

  • cortisol increased

  • ACTH increase by the ant. pit. results in the adrenal cortex production of cortisol to increase and vice versa

• Addison’s Disease= primary hypocortisolism

  • problem with the adrenal cortex

  • hypocortisolism paired with hypoaldosteronism

  • results in a deficit of both aldosterone and cortisol

  • could result from suddenly stopping the intake of steroid drugs

    • takes months for the cortex to “wake up” following their use

    • called an Adisonian crisis

    • Memory trick story: “Addison lost cortisol at the same time that Ian lost his aldosterone and now both Cries out for help”

    • the reason why we ALWAYS taper off of steroids

    • the reason why we NEVER abruptly stop taking steroids

Aldosterone

• what does this hormone do?

  • lower K

  • higher Na

  • higher BV

  • higher BP

• RAAP= renin-angiotensin-aldosterone-pathway

  • renin turns angiotensinogen into angiotensin 1

  • ACE converts angiotensin 1 into angiotensin 2

  • angiotensin 2 stimulates the release of aldosterone

  • aldosterone stimulates constriction of blood vessels

• RENIN MUST BE RELEASED FOR ALDOSTERONE TO BE!!!

  • without renin release, the RAAP doesn’t happen

  • renin is usually released by kidneys in response to low blood pressure or low sodium levels

• 1* hyper= renin decrease

• 2* hyper= renin increase

• 1* hypo= renin increase

• 2* hypo= renin decrease

Hypoaldosteronism

• is not always Addison’s Disease

• low aldosterone levels

• what are some common effects?

  • These are common in BOTH 1* and 2*

    • hyperkalemia

      • due to the aldosterone not getting rid of K

    • hyponatremia

      • due to aldosterone not having the body retain it

    • hypovolemia

      • due to aldosterone not causing Na retention to keep the water in the blood resulting in a decreased blood volume

• primary is due to an adrenal cortex problem

  • the aldosterone is low but renin high

• secondary is due to a problem with the RAAP

  • the aldosterone low and renin low

• How do we determine if primary or secondary?

  • we look at the Renin levels!!!

  • Ask: “Is this the expected response?”

• Patient 1:

  • ALDO low

  • Renin high

  • the renin is doing what it’s supposed to BUT the aldosterone is still low so the cause is an adrenal problem

  • pt has primary hypoaldosteronism

• Patient 2:

  • ALDO low

  • Renin low

  • The renin NOT stimulating the release of aldosterone, so the cause is a RAAP issue

  • pt has secondary hypoaldosteronism

Hyperaldosteronism

• what are some common effects?

  • the are common in BOTH 1* and 2*

    • hypokalemia

      • due to the aldosterone getting rid of too much

    • increased BV

      • due to retaining more Na resulting in more water in the blood

    • increased BP

      • due to the increase in blood volume

• high levels of aldosterone

• would expect a decrease in Renin levels

• Primary is caused by an adrenal problem

  • also called Conn’s Disease

• Secondary is caused by a RAAP problem

• Patient 1:

  • ALDO high

  • Renin high

  • the Renin is causing an abnormal increase in aldosterone

  • pt has secondary (2*) hyperaldosteronism

• Patient 2:

  • ALDO high

  • Renin low

  • RAAP is reacting appropriately but the adrenals are not decreasing the amount of aldosterone

  • means there’s a glad issue

  • pt has primary (1*) hyperaldosteronism = Conn’s Disease

DM= Diabetes Mellitus

• is a disorder related to insulin: either the absence of it or a resistance to it by the target receptors

• type 1= low insulin

• type 2= tissue resistance to insulin/ decreased tissue sensitivity to insulin

• a disorder related to hyperglycemia= high glucose levels in the blood

• what is the typical clinical presentation of diabetes?

  • polyuria

    • excessive urination

    • due to the kidneys trying to pee off the excess glucose in the blood

  • polydipsia

    • excessive thirst

    • due to the polyuria and decrease in ECF dilution because excess glucose increases the concentration

  • polyphagia

    • excessive hunger

    • due to too much sugar staying in the blood and not going into the cells to provide the body with energy

  • weight loss

• what are the “three P’s” of diabetes?

  • polyuria, polydipsia, and polyphagia

• Does one ever stop being diabetic?

  • NO! Once you are diagnosed, you are diabetic for the rest of your life

• How do we treat DM?

  • goal is to minimize the hyperglycemia by maximizing the control of blood glucose

  • diet

  • exercise

  • medication

  • watching sugar intake

• The measure of long-term glucose control is the hemoglobin A1C

  • a higher % = less control over

    • normal range is less than 5.4%

    • prediabetic is around 5.5-5.7%

    • good control is equal to or less than 7.0%

• without tight glucose control complications occur which can even be life-threatening

• What are complications common to both types?

  • macrovascular

    • think arteries

    • due to prolonged uncontrolled glucose levels

    • all associated with atherosclerotic plaques in the vessels

      • often form in many locations throughout the body

      • more poorly controlled DM results in a higher risk of plaque formation

    • CAD= coronary artery disease

      • associated with MI (heart attack) risk

    • CVD= cerebrovascular disease

      • associated with stroke risk

    • PAD= peripheral artery disease

      • associated with limb amputation risk

  • microvascular

    • think capillaries

    • retinopathy

      • the capillaries of the eyes

      • is a chronic condition

      • often associated with new-onset blindness

      • why a DM pt should get annual eye exams!!!

    • nephropathy

      • is a kidney issue

      • associated with chronic kidney failure

    • neuropathy

      • a nerve issue

      • often peripheral

      • can be painless or painful

Type 1

• absolute insulin deficit

  • due to beta cell destruction

• can be treated by giving pt insulin injections

  • give them what their body is not producing

Type 2

• relative insulin deficit

  • the beta cells of the pancreas are impaired

• some level of tissue resistance to insulin

• some of the hormone is produced, but it’s paired with the tissues being resistant to the insulin

• many patients take medication to either increase production, decrease resistance, or both

• some less severe cases can be treated through diet and exercise alone

• VERY COMMON!!!

  • about 90% of all diabetics are Type 2