systemic pathology 400 (CV class 4) Flashcards

1
Q

telangiectasis

A

aka “ spider veins”

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2
Q

what are spider veins (telangiectasia)

A

Vascular lesion formed by dilation of a group of small blood vessels

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3
Q

where can spider veins occur? whre are they most common

A

Can occur anywhere on the skin

Most frequently seen on the face and thighs

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4
Q

is spider veins a serious issue

A

generally just a cosmetic condition –> generally no functional effect on health

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5
Q

how can spider veins appear?

spider veins vs childhood

A

May appear as a birthmark or become apparent in young children

“Spider telangiectasias are fairly common and look like little red lines on a child’s skin. They are usually nothing more than a cosmetic problem. They form as a result of abnormal blood vessels (a.k.a. a vascular anomaly). Spider telangiectasias don’t cause any health problems.”

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6
Q

risk factors / associated factors (telangiectasis)

A

May be associated with

long term sun exposure,
standing,
age,
varicose veins,
gender,
pregnancy,
trauma,
steroid treatment,
rosacea, etc.

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7
Q

telangiecstasis etymology

A

telos = end

angeion = vessel

ektasis = dilatation

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8
Q

frostbite

A

Localized medical condition whereby damage is caused to skin and other tissues due to extreme cold.

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9
Q

frostbite – etiology / risk factors

A

Extreme cold/wind chill
Wet clothes
Poor circulation
Blood vessel d/o
Low body fat
Age
Medications
Smoking, alcohol, drugs
Homelessness

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10
Q

frostbite – pathogenesis

A

Vasoconstriction upon exposure to cold

—> This helps to preserve core body temperature

Ice crystals form in tissues and expand into extracellular spaces
—> cell membrane rupture
—> disruption of enzyme activity
—> tissue death

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11
Q

retrostasis vs hunting response

A

retrostasis at first

hunting response after 10-15 or 20 (?) minutes
—> alternating vasodilation/constriction to prevent superficial tissue damage

when cold continue however, – body goes back to RETROSTASIS –> b/c the vital organs need to maintain temperature to prevent death

—> thus superficial tissue loses blood supply, and can die d/t anoxia

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12
Q

frostbite classification

(superficial classification)

A

Superficial frostbite affects skin and subcutaneous tissue

—> Discoloration of the skin, burning and/or tingling, swelling

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13
Q

(deep frostbite)

A

Deep frostbite extends beyond the superficial tissue

—> White skin, pain, blisters, tissue necrosis, gangrene

—> ultimately turns black (?) when dead

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14
Q

frostbite Dx

A

Based on history and clinical presentation

Bone scan

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15
Q

frostbite and bone scan

A

if frostbite/necrosis has reached bone –> then amputation must take place

“It is concluded that scintigraphy is an excellent means of evaluating patients with severe frostbite of the extremities: as early as day 2 after the injury it can indicate whether amputation is necessary, and between days 2 and 8 it provides valuable information on the efficacy of treatment.”

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16
Q

scintigraphy

A

a technique in which a scintillation counter or similar detector is used with a radioactive tracer to obtain an image of a bodily organ or a record of its functioning.

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17
Q

frostbite tx

A

Vasodilators

Rewarm the area without rubbing or massaging
—> Reperfusion injury is a serious complication

Pain meds

Surgery, amputation

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18
Q

reperfusion ?

A

“Reperfusion is the restoration of blood flow to an organ or tissue after having been blocked, and may refer to: Reperfusion injury, tissue damage caused when blood supply returns to the tissue.

Reperfusion therapy, the medical treatment that restores blood flow through blocked arteries, typically after a heart attack.”

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19
Q

why does reperfusion cause tissue damage

A

The inflammatory response is partially responsible for the damage of reperfusion injury. White blood cells, carried to the area by the newly returning blood, release a host of inflammatory factors such as interleukins as well as free radicals in response to tissue damage.

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20
Q

diabetic microangiopathy

A

Years of poorly controlled hyperglycemia leads to vascular complications that affect small (microvascular) vessels, large (macrovascular) vessels, or both.

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21
Q

pathogenesis (diabetic microangiopathy)

A

Vascular disease due to:

Glycosylation of serum and tissue proteins

Superoxide production

Activation of signaling molecules
—> increase vascular permeability
—> endothelial dysfunction

Hypertension

Arterial microthromboses

Hyperglycemia/hyperinsulinemia
—> inflammation and prothrombotic effects
—> impaired vascular autoregulation

Hyperglycemia
—> impaired cellular immunity
—> immune dysfunction

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22
Q

glycoxidation

A

“Glycoxidation is a process whereby glycated proteins chemically generate oxygen free radicals.”

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23
Q

why superoxide production

A

However, in diabetic conditions, the uncoupling of eNOS in diabetic vascular endothelial cells leads to the overproduction of superoxide anion (O2* −), which decreases NO availability, impairs the endothelium and ultimately increases superoxide in blood vessels [23].

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24
Q

1) diabetic microangiopathy VS Diabetic retinopathy

A

No early symptoms or signs, but blurring, retinal detachment, and partial or total vision loss eventually develop

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25
diabetic retinopathy is...
Most common cause of adult blindness in the US
26
2) diabetic microangiopathy vs Diabetic neuropathy
The result of nerve ischemia from microvascular disease, direct effects of hyperglycemia on neurons, and intracellular metabolic changes that impair nerve function
27
diabetic retinopathy pathogenesis (?)
The pathologic process involved in DME is the resultant fluid leaking into the retina and depositing under the macula. Sediment left behind from this edema leads to waxy, yellow lipid byproducts referred to as hard exudates. (Diabetic macular edema (DME))
28
diabetic nephropathy
Involves glomerular sclerosis and fibrosis caused by the metabolic and hemodynamic changes of diabetes
29
diabetic nephropathy is
The number one cause of renal failure in the US
30
note about diabetic neuropathy (as a result of diabetic microangiopathy)
also recall CHARCOT'S neuropathy
31
decompression sickness
AKA caisson disease, the bends, divers disease
32
what is decompression sickness?
Decompression sickness occurs when rapid pressure reduction (e.g. during ascent from a dive, or ascent to altitude) causes gas previously dissolved in blood or tissues to form bubbles in blood vessels.
33
decompression sickness and Henry's law
The solubility of a gas in a liquid is directly proportional to the pressure exerted on the gas and liquid.
34
steps during decompression sickness
during descent (diving) ---> nitrogen moves from high pressure in lungs too blood (low pressure) swimming up too quickly doesn't give nitrogen enough time to leave blood ---> forms bubbles that lead to SSx whereas a slow ascent would let the nitrogen gradually return to lungs where it is breathed out
35
decompression sickness -- incidence
Approximately 2 to 4/10,000 dives Men > women
36
decompression sickness -- RISK FACTORS
Cold temperature dives Prolonged or deep dives Rapid ascent Dehydration Flying after diving Obesity Older age
37
why is it called the bends?
DCS often causes air bubbles to settle in major joints like knees or elbows, causing individuals to bend over in excruciating pain, hence its common name, the bends.
38
caisson
a large watertight chamber, open at the bottom, from which the water is kept out by air pressure and in which construction work may be carried out under water.
39
why called caisson disease
The original name for DCS was "caisson disease". This term was introduced in the 19th century, when caissons under pressure were used to keep water from flooding large engineering excavations below the water table, such as bridge supports and tunnels.
40
decompression sickness SSx
Dependent on which tissue is affected: Joint and muscle pain N/V dyspnea (shortness of breath) Numbness, tingling, formication Seizures Itching and/or rash Hearing loss
41
formication define
Formication is a symptom where you hallucinate the feeling of insects crawling in, on or under your skin. This symptom can be very upsetting or disturbing, leading to other issues like self-injury from scratching or trying to get the insects out from under or inside of your skin.
42
decompression sickness -- dx, tx
Diagnosis History and clinical manifestation Treatment Oxygen chamber and recompression therapy
43
decompression sickness -- px
Prognosis About 80% of patients recover completely 20% may have long term / chronic SSx
44
varicose veins aka
AKA varicosities
45
what are varicose veins?
An abnormal dilation of veins leading to tortuosity (twisting and turning) of the vessel, incompetence of the valves, and a propensity to thrombosis
46
varicose veins incidence
Women are affected more often than men (secondary to pregnancy) until 70 y.o. 70% of women ages 60-70 have varicose veins Usually develops between ages 30-50
47
varicose veins risk factors
Periods of high venous pressure associated with: Heavy lifting Prolonged sitting or standing Hormonal changes Menopause Pregnancy Heart failure Constipation (hemorrhoids) Hereditary factors* CT disease Valvular incompetence Obesity
48
varicose veins common sites
Lower extremity Saphenous vein Rectum and anal canal – hemorrhoids (can be internal or external) Scrotum - varicocele
49
varicocele risk factors
age genetics anatomy testicular growth physical exertion sedentary lifestyle occupation body weight heat exposure infertility
50
varicose veins genreally @
superficial veins
51
varicose veins -- clinical manifestations
The clinical picture is not correlated with the severity of the varicosities The development of varicose veins is gradual. Most are asymptomatic (perhaps with the exception of hemorrhoids)
52
most common symptom of varicose veins (when symptomatic)
The most common symptom is dull, aching heaviness, tension, or fatigue brought on by standing.
53
varicose veins of scrotum (varicocele)
could be d/t serous fluid production in scrotum
54
"The clinical picture is not correlated with the severity of the varicosities"
I.e. a tiny varicosity could be painful and achy & large amounts of varicosities could be asymptomatic (Recall, similar to osteoarthritis -- amount of wear/damage does not necessarily correlate to SSx/pain)
55
varicose veins -- other notes about clinical manifestations
Clinical Manifestation: Cramps are relieved with elevation of legs Itching may occur The veins are dilated, tortuous and elongated beneath the skin
56
secondary changes of varicose veins
Secondary changes include browning and swelling Veins may become thick and hard to the touch
57
varicose veins -- complicaitons
Ulcers due to compromised circulation Thrombosis Inflammation of the vein - phlebitis
58
how can varicose veins lead to phlebitis
A common pathway for developing phlebitis is when a clot develops in a varicose vein, just underneath the skin surface. Symptoms of phlebitis are caused by inflammation, which represents the body's response to injury or tissue damage. Phlebitis can be triggered by excessive stretching of the leg veins.
59
venous thrombosis
..
60
venous thrombosis define
Venous thrombosis - partial or full occlusion of a vein by a clot
61
phlebothrombitis
inflammation of a vein, predisposing a person to clot formation (also note form previous card -- clot can lead to inflammation, and inflammation can lead to clot (?)
62
thrombophlebitis
partial or complete occlusion of a vein by a thrombus (clot) with a secondary inflammatory reaction in the wall of the vein
63
thrombophlebitis vs phlebothrombitis
"Thrombophlebitis is a condition in which inflammation of the vein wall has preceded the formation of a thrombus (blood clot). Phlebothrombosis is the presence of a clot within a vein, unassociated with inflammation of the wall of the vein (Fig. 27.6)." ---> NOTES DIFFERENT = inflammation is risk factor for the clot vs above: "clot within a vein, unassociated with inflammation of the wall"
64
venous thrombosis -- Classificaiotn
superficial vs deep
65
deep venous thrombosis
Deep (DVT) Usually present in the calf. It is often clinically silent and benign although complications can lead to pulmonary emboli. Thromboses in the popliteal, femoral, iliac veins or inferior vena cava are associated with greater risk of PULMONARY EMBOLISM
66
which DVT locaitons are risk factors for pulmonary embolism
popliteal, femoral, iliac veins or inferior vena cava
67
venous thrombosis -- etiology and risk factors
Surgery – most common Genetics Oral contraceptives Smoking Venous stasis Hypercoagulability of blood
68
venous thrombosis -- incidence
DVT is the third most common CV disease after coronary artery episodes (heart attack) and cerebrovascular accidents (stroke). 2 million Americans die of DVT per year
69
DVT mechanism of death
Deep vein thrombosis can be serious because blood clots in the veins can break loose. The clots can then travel through the bloodstream and get stuck in the lungs, blocking blood flow (pulmonary embolism). When DVT and pulmonary embolism occur together, it's called venous thromboembolism (VTE).
70
venous thrombosis pathogenesis
Trauma to endothelium of the vein exposes subendothelial tissue to platelets and clotting factors, initiating thrombosis Platelets adhering to vessel wall attract fibrin, leukocytes, erythrocytes Clot can undergo recanalization, dissolution, organization, or can persist as a thrombus or break free and become an embolus
71
venous thrombosis -- clinical manifestation
Variable and inconsistent Asymptomatic LE>UE Edema Dull ache Tightness, tenderness Swelling
72
venous thrombosis Dx
Based on signs, symptoms and risk factors Ultrasound
73
venous thrombosis -- Tx
Elastic stockings (COMPRESSION SOCKS) Medications Surgery
74
why do compression socks help with venous thrombosis?
Compression socks, which are made from synthetic materials, are tighter than regular socks. They apply controlled pressure to improve blood flow in the veins of the leg. There are medical-grade compression stockings that are “graduated”—tightest at the ankles, with the compression gradually easing up the legs. "The compression of the socks gently pushes blood flow up the leg, helping to prevent swelling and even blood clots."
75
venous stasis
AKA postphlebitis syndrome, chronic venous insufficiency
76
postphlebitis syndrome vs post-thrombotic syndrome
Post-thrombotic syndrome refers to symptoms and signs of chronic venous insufficiency that develop following deep vein thrombosis (DVT) and is a common, burdensome, and costly complication [1,2]. The term "post-thrombotic" replaces the prior terminology "postphlebitic" syndrome ** "Immediate compression and walking seems also to reduce the incidence of a postthrombotic syndrome." (w/ respect to compression socks and venous thrombosis)
77
so what is venous stasis?
Inadequate venous return over a long period of time
78
VENOUS STASIS -- two relevant risk factors
venous thrombosis and varicose veins
79
venous stasis and venous thrombosis
Venous stasis syndrome is typically considered a long-term sequel of deep vein thrombosis (DVT; also known as post-thrombotic syndrome or post-phlebitic syndrome in the post-DVT setting). The cumulative incidence of venous stasis syndrome after DVT is 20–50%, with a third being severe venous stasis syndrome4–9. Note: that's why venous stasis is aka post-thrombotic synrome
80
venous stasis and varicose veins
Conclusions. Increasing patient age and BMI, prior DVT (particularly left leg DVT), longer time interval since DVT and varicose veins are independent risk factors for venous stasis syndrome.
81
venous stasis typically follows...
Follows most severe cases of DVT
82
venous stasis can also occur secondary to
varicose veins, leg trauma, or neoplasms
83
venous stasis -- clinical manifestations
Progressive edema of the leg Thickening, coarsening, and brownish pigmentation of the skin around the ankles (stasis dermatitis) Venous stasis ulceration ---> Painful, shallow wounds ---> Large amounts of drainage
84
stasis dermatitis (note individuals with brown ankles)
Stasis dermatitis involves skin changes that are caused by poor circulation and the resulting pooling of blood in the lower legs. Also called gravitational dermatitis and venous eczema, this condition could develop with aging, but it could also indicate the presence of another condition, like kidney or heart disease.
85
venous stasis -- Dx & Tx
Diagnosis: History and examination Treatment: Treatment is as for varicose veins. Prognosis: Poor
86
Treatment: Treatment is as for varicose veins.
Rest and elevation Exercise Elastic stockings (COMPRESSION SOCKS) Surgery, if necessary
87
venous stasis aka
chronic venous insufficiency
88
Raynaud's
Raynaud’s disease: Occurs on its own and isn’t connected with another disease or condition. This is also called primary Raynaud’s syndrome. Raynaud’s phenomenon: Occurs due to an underlying condition, medication or lifestyle factor. This is also called secondary Raynaud’s syndrome. Raynaud’s syndrome: Refers to either the primary or secondary form of the condition.
89
Raynaud's is
Intermittent episodes of small artery or arteriole constriction of the extremities causing temporary pallor and cyanosis of the digits and changes in skin temperature
90
why does Raynaud's take place
Occurs in response to cold temperature, anxiety or excitement
91
Primary Vasospastic Disorder (Raynaud’s Disease)
Idiopathic
92
Raynaud’s Phenomenon
Secondary to another disease or underlying cause
93
RAYNAUD’S -- incidence / risk factors
Usually more common in women Age Smoking, alcohol may be a factor.
94
Raynaud's can also be associated with
occlusive arterial disease, neurogenic lesions, TOS, frostbite, trauma, the chronic use of vibrating equipment, repetitive stress injuries to the small vessels of the hands,
95
vibration Raynaud's
Vibration white finger is a type of secondary Raynaud's phenomenon. In this type, blood vessels, nerves, and other tissue become damaged due to chronic vibration.
96
also a known risk factor
Possibly a disturbance in the control of vascular reflexes ---> overactive sympathetic nervous system in that area ---> vasoconstriction
97
Raynaud's clinical manifestation
White, blue, then red digits ---> MORE OFTEN IN UE than LE Throbbing, paresthesia, swelling ---> Sensory changes, such as numbness, stiffness, diminished sensation, aching pain often occur.
98
what can prolonged Raynaud's do to hands/fingers
Over time, frequent prolonged episodes can cause the fingertips to thicken and the fingernails to become brittle.
99
Raynaud's typical phases
phase 1: Ischemia phase 2: Cyanosis phase 3: Rubor
100
Raynaud's Dx
Diagnosis based on clinical presentation and history
101
Raynaud's disease (primary Raynaud's) Dx
Raynaud’s disease – history of symptoms for at least 2 years with no progression and no evidence of underlying cause (idiopathic)
102
Raynaud's Tx
Avoid triggers Decrease smoking Physical therapy Relaxation techniques Exercise Heat
103
Raynaud's Px
Untreated and uncontrolled Raynaud’s may damage or destroy affected digits. (long term) Disability and loss of function can occur. RECALL: "Over time, frequent prolonged episodes can cause the fingertips to thicken and the fingernails to become brittle. "
104